PsychoPharmRef

A clinical psychopharmacology reference for psychiatrists, residents, and students — drug data, interaction checkers, rating scales, printable forms, patient handouts, and evidence-based chapters, all in one place.

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Searchable drug database, CYP450 interaction checker, receptor binding profiles, and PK curve comparisons.

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Drug Database

Show all columns

Sort by side effect risk:

Drug	Risk	Class	IBH Ref	Active Enantiomer	Half-Life (Parent)	Active Metabolites	Renal Adjust	Hepatic Adjust	Geriatric	QT Prolongation	Lipid ↑ Risk	Glucose ↑ Risk	EPS Risk	Protein Binding	Pregnancy	Breastfeeding	Route	Pre / Post-Synaptic Binding	Receptor Chart

P450 Interactions

CYP enzyme interactions for all medications. S = Substrate • Inhibitor strength shown in color • Ind = Inducer

S Substrate Inh-S Strong Inhibitor Inh-M Moderate Inhibitor Inh-W Weak Inhibitor Ind Inducer

Filter by category:

Drug	Class	CYP1A2	CYP2B6	CYP2C9	CYP2C19	CYP2D6	CYP3A4

Receptor Binding Profiles

Ki values in nM (lower = higher affinity). Pie shows relative affinity (1/Ki normalized). Bar charts show pKi = −log₁₀(Ki) per drug class.

Select Drug:

Select a drug above to see its receptor binding profile.

Side-by-Side Drug Comparison

Select any two medications to compare their receptor binding profiles directly.

Drug A

vs

Drug B

Class Comparisons — pKi by Receptor

Each chart shows all drugs in a class. Y-axis: pKi = −log₁₀(Ki nM). Higher bar = stronger affinity. Switch to treemap view for an area-based hierarchy that can be easier to compare across many drugs.

Drug Class:

Receptor Glossary

Clinical effects of receptor activation or inhibition. Expand any receptor for a full breakdown of benefits and side effects.

Psychiatry Glossary

A working clinical dictionary of psychiatry-specific language — phenomenology, diagnoses, defense mechanisms, eponyms, scales, and neuroanatomy. Search above for instant definition previews.

0 terms

Pharmacokinetic Curve Comparison

Compare estimated plasma concentration curves across medications. Select a category, then choose up to 8 drugs to overlay. Peak height is scaled by primary receptor binding affinity (lower Ki = stronger binding = taller peak). The dot on each curve marks one half-life after peak concentration.

References & Methods

Data sources, methodology, and direct FDA labeling access.

🔍 FDA Drug@FDA Search

Search the official FDA Drug@FDA database directly at accessdata.fda.gov. Enter any medication name to open its FDA labeling page.

⚙ Methods — How Data Is Calculated

Receptor Binding Affinity (Ki Values)

Receptor binding data is expressed as the inhibition constant Ki (nM) — the concentration of drug required to occupy 50% of a receptor in a competitive binding assay. Lower Ki values indicate stronger binding affinity. All Ki values are sourced from in vitro radioligand binding studies, primarily the NIMH Psychoactive Drug Screening Program (PDSP) database, FDA-approved prescribing information, and peer-reviewed pharmacology literature.

Ki values of ≥10,000 nM are treated as negligible affinity and displayed as "—" in charts. For visualization, Ki is converted to pKi using the formula:

pKi = 9 − log₁₀(Ki_nM)

This transforms Ki in nanomolar units to the equivalent of −log₁₀(Ki in molar), producing values typically between 5 and 10 where higher numbers indicate stronger binding. The pie chart displays relative affinity normalized from 1/Ki values (receptors with Ki ≥5,000 nM excluded).

Side Effect Risk Scores

Side effect risk scores estimate the likelihood that a drug will cause a given clinical side effect based on its receptor binding profile. Scores range from 0 to 100 (higher = greater predicted risk) and are calculated as follows:

Receptor-to-side-effect mapping: Each side effect is linked to one or more receptors known to mediate it, each assigned a clinical weight (0–1.0) based on the strength of the pharmacological evidence. For example, sedation is driven primarily by H₁ antagonism (weight 1.0), with secondary contributions from α₁ (0.5) and M₁ (0.3).
Affinity normalization: For each relevant receptor, the drug's Ki value is converted to a 0–1 affinity score using the pKi scale: normalized = max(0, (pKi − 5) / 4). This maps the range Ki=10,000 nM (pKi=5 → score 0) to Ki=1 nM (pKi=9 → score 1). Drugs with Ki ≥10,000 nM score 0.
Weighted average: The final score is the weighted average of normalized affinity scores across all receptors in the profile, multiplied by 100: Score = (Σ weight × normalized) / Σ weight × 100.
Risk thresholds: Scores are binned as: Very Low (<20), Low (20–39), Moderate (40–59), High (60–79), Very High (≥80).

Side Effect	Receptor Drivers (weight)
Sedation / Drowsiness	H₁ (1.0), α₁ (0.5), M₁ (0.3)
Weight Gain	H₁ (1.0), 5HT₂C (0.9), M₁ (0.2)
Dry Mouth / Constipation	M₁ (1.0)
Orthostatic Hypotension	α₁ (1.0), α₂ (0.3)
Sexual Dysfunction	SERT (1.0), 5HT₂A (0.4)
EPS / Akathisia	D₂ (1.0), D₃ (0.5)
Metabolic Effects	5HT₂C (1.0), H₁ (0.8), M₁ (0.2)
Insomnia / Activation	DAT (1.0), NET (0.9), SERT (0.3)
Hyperprolactinemia	D₂ (1.0)
Nausea / GI Upset	SERT (0.8), D₂ (0.6)
Cognitive Impairment	M₁ (1.0), H₁ (0.7), α₁ (0.3)
Cardiac / QT Effects	H₁ (0.5), α₁ (0.6)

⚠ Important caveat: Side effect scores are derived from in vitro receptor binding data and represent a pharmacological prediction — not a clinical probability. They do not account for pharmacokinetic factors (bioavailability, CNS penetration, active metabolites), dose-dependence, individual patient variability, or clinical trial incidence data. Scores should be interpreted as a comparative tool to guide discussion, not as definitive risk estimates.

Antipsychotic Lipid, Glucose & EPS Risk Columns

When the drug database is filtered to Antipsychotics, three additional columns appear: Lipid ↑ Risk, Glucose ↑ Risk, and EPS Risk. Unlike the receptor-affinity side-effect scores above, these are curated per-drug tiers (Very Low → Very High) drawn directly from comparative clinical trial data, because lipid and glucose effects diverge from in vitro receptor binding and are best separated using head-to-head evidence.

Lipid ↑ and Glucose ↑: Ranked primarily from the metabolic network meta-analysis of 18 antipsychotics by Pillinger et al. (2020), which reports separate effects on lipids and fasting glucose — olanzapine and clozapine carry the greatest risk on both, while aripiprazole, brexpiprazole, cariprazine, lurasidone, ziprasidone, lumateperone and pimavanserin are most benign. Lipid and glucose are rated independently (e.g. quetiapine: higher lipid than glucose; risperidone/paliperidone raise lipids/weight without substantial fasting-glucose elevation).
EPS Risk: Reflects extrapyramidal / movement-disorder liability from comparative data (Leucht et al. 2013; Huhn et al. 2019), tracking antipsychotic potency — high-potency first-generation agents (haloperidol, fluphenazine, pimozide) highest; clozapine, quetiapine, lumateperone and pimavanserin lowest.

⚠ Important caveat: These tiers are a comparative, class-level guide for educational use. Actual risk is dose-dependent and modified by individual patient factors, duration of exposure, and baseline metabolic status; always verify against current prescribing information and monitoring guidelines.

Pregnancy & Breastfeeding Data

Pregnancy classifications use the historical FDA letter category system (A/B/C/D/X), which remains widely referenced clinically despite being replaced by the Pregnancy and Lactation Labeling Rule (PLLR) for drugs approved after 2015. Drugs approved under PLLR are labeled "N/A" for category.

Breastfeeding classifications use Hale's Lactation Risk Categories (L1–L5):

L1 — Safest: Extensively studied; no adverse effects in infant; not orally bioavailable in infant.
L2 — Safer: Limited studies show no increase in adverse effects; risk to infant is remote.
L3 — Moderately Safe: No controlled studies; risk of adverse effects possible; give only if benefit outweighs risk.
L4 — Possibly Hazardous: Positive evidence of risk to infant; benefits may be acceptable in life-threatening situations.
L5 — Contraindicated: Risk clearly outweighs any benefit.

Sources: FDA prescribing information, NIH LactMed database, Hale's Medications and Mothers' Milk (2023), Briggs Drugs in Pregnancy and Lactation (12th ed.).

QTc Calculator & Tisdale Risk Score

QTc values are calculated using the Bazett formula (QTc = QT / √RR) and the Fridericia formula (QTc = QT / ∛RR), where RR = 60/HR in seconds. Fridericia is recommended at heart rates <50 or >100 bpm as Bazett over-corrects at extremes.

The Tisdale Risk Score is reproduced from: Tisdale JE, et al. Circ Cardiovasc Qual Outcomes. 2013;6(4):479–487. It was validated in hospitalized patients; application in outpatient settings should be interpreted with appropriate clinical judgment.

📚 General References

NIMH Psychoactive Drug Screening Program (PDSP) Ki Database. pdsp.unc.edu
FDA Drug@FDA Database. accessdata.fda.gov
NIH LactMed Database. nlm.nih.gov/lactmed
Stahl SM. Stahl's Essential Psychopharmacology: Neuroscientific Basis and Practical Applications. 5th ed. Cambridge University Press; 2021.
Hale TW. Medications and Mothers' Milk. 2023 ed. Springer; 2023.
Briggs GG, Freeman RK, Towers CV, Forinash AB. Drugs in Pregnancy and Lactation. 12th ed. Wolters Kluwer; 2021.
Tisdale JE, et al. Development and validation of a risk score to predict QT interval prolongation in hospitalized patients. Circ Cardiovasc Qual Outcomes. 2013;6(4):479–487.
Pillinger T, McCutcheon RA, Vano L, et al. Comparative effects of 18 antipsychotics on metabolic function in patients with schizophrenia, predictors of metabolic dysregulation, and association with psychopathology: a systematic review and network meta-analysis. Lancet Psychiatry. 2020;7(1):64–77. thelancet.com
Huhn M, Nikolakopoulou A, Schneider-Thoma J, et al. Comparative efficacy and tolerability of 32 oral antipsychotics for the acute treatment of adults with multi-episode schizophrenia: a systematic review and network meta-analysis. Lancet. 2019;394(10202):939–951.
Leucht S, Cipriani A, Spineli L, et al. Comparative efficacy and tolerability of 15 antipsychotic drugs in schizophrenia: a multiple-treatments meta-analysis. Lancet. 2013;382(9896):951–962.
Academy of Consultation-Liaison Psychiatry (ACLP). How-To Guide: QTc Prolongation. 2020.
Woosley RL, Heise CW, Gallo T, et al. CredibleMeds / AZCERT QTDrugs List. crediblemeds.org
Roden DM. Drug-induced prolongation of the QT interval. N Engl J Med. 2004;350:1013–1022.
Drew BJ, et al. Prevention of Torsade de Pointes in Hospital Settings. Circulation. 2010;121:1047–1060.

QT Prolongation Risk Tool

QTc calculator, Tisdale risk scoring, drug reference lists, and monitoring guidance. For educational use — always verify with current clinical resources.

What Is QT Prolongation?

The QT interval on an ECG represents ventricular depolarization (QRS) plus repolarization (T wave). Prolongation of the QT interval reflects delayed ventricular repolarization, creating a vulnerable window during which an early depolarization can trigger a potentially fatal arrhythmia.

Because the QT interval varies with heart rate, a corrected QTc is calculated to normalize for rate. The most widely used formula is Bazett's, though Fridericia's is preferred at very high or low heart rates.

Bazett (most common)

QTc = QT ÷ √RR

RR in seconds = 60 ÷ HR

Fridericia (preferred at HR <50 or >100)

QTc = QT ÷ ∛RR

More accurate across heart rate extremes

QTc Thresholds

≤440 ms

Normal (men)

≤450 ms

Normal (women)

450–470 ms

Borderline — monitor

>470 ms (♀) / >450 ms (♂)

Prolonged — review agents

≥500 ms

High risk — TdP threshold

+60 ms from baseline

Clinically significant change

Torsades de Pointes (TdP) & Risk Factors

Torsades de Pointes (TdP) is a polymorphic ventricular tachycardia characterized by a "twisting" QRS morphology around the isoelectric axis. It can degenerate into ventricular fibrillation and sudden cardiac death.

Patient-Level Risk Factors

Female sex — longer baseline QTc; ~70% of TdP cases
Age ≥65 — reduced repolarization reserve
Hypokalemia (K+ <3.5 mEq/L) — most important electrolyte
Hypomagnesemia — Mg²⁺ <0.8 mEq/L
Hypocalcemia
Bradycardia (<50 bpm) — rate-dependent TdP risk

Heart failure — reduced repolarization reserve
Myocardial infarction / ischemia
Congenital long QT syndrome
Hypothyroidism
Hepatic impairment — increases drug exposure
Anorexia nervosa — electrolyte depletion

Additive risk: The combination of multiple QT-prolonging drugs is the most common preventable cause of drug-induced TdP. Two drugs with modest individual risk can produce synergistic QTc prolongation when co-prescribed.

Monitoring Recommendations

Before Starting a QT-Prolonging Agent

Obtain baseline ECG with QTc measurement
Review all concurrent medications for additive QT risk (CredibleMeds / AZCERT database)
Measure and correct electrolytes (K⁺, Mg²⁺, Ca²⁺) before initiation
Assess for congenital long QT syndrome risk (family/personal history of sudden death, syncope)
Assess renal and hepatic function — affects drug clearance and exposure

During Treatment

Repeat ECG 1–2 weeks after initiation and after dose increases
For high-risk agents (e.g., methadone, haloperidol IV, clozapine): ECG at 1 week, 1 month, then periodically
Monitor electrolytes regularly, especially with diuretics, vomiting, or poor oral intake
Educate patient on symptoms: palpitations, dizziness, syncope, presyncope

Action Thresholds

450–499 ms

Correct electrolytes; reassess drug necessity; increase monitoring frequency

500–519 ms

Reduce dose or discontinue offending agent(s); cardiology consultation

≥520 ms or +60 ms

Discontinue QT-prolonging agent(s); urgent cardiology evaluation; consider inpatient monitoring

Note on CredibleMeds: The Arizona CERT / CredibleMeds database (crediblemeds.org) is the authoritative resource for drug-induced QT risk classification. Categories include: Known Risk, Conditional Risk, Possible Risk, and Special Risk. Clinicians should consult this database for the most current risk listings.

▶ QTc Calculator

Enter the measured QT interval and heart rate from the ECG. QTc is calculated using both Bazett and Fridericia formulas.

QT Interval (ms)

Heart Rate (bpm)

Patient Sex

▶ Non-Psychiatric Medications with QT Risk

Commonly prescribed medications outside psychiatry that prolong the QT interval. Risk classification based on CredibleMeds / AZCERT and published literature. This does not replace the CredibleMeds database — always verify current risk status.

Known Risk Established evidence for QT prolongation and TdP | Conditional Risk under certain conditions (dose, drug interactions, patient factors) | Possible Some evidence but less established

▶ Psychiatric Medications with QT Risk

Medications in the database flagged for QT prolongation. Click any drug name to open its full detail modal.

▶ References

Tisdale JE, et al. Development and validation of a risk score to predict QT interval prolongation in hospitalized patients. Circ Cardiovasc Qual Outcomes. 2013;6(4):479–487.
Tisdale JE, et al. Drug-Induced QT Interval Prolongation and Torsades de Pointes: Role of the Pharmacist in Risk Assessment, Prevention and Management. Can Pharm J (Ott). 2016;149(3):139–152.
Academy of Consultation-Liaison Psychiatry (ACLP). How-To Guide: QTc Prolongation. 2020. Available at: aclponline.org.
Woosley RL, Heise CW, Gallo T, et al. CredibleMeds / AZCERT. Available at: crediblemeds.org. [QTDrugs List — updated continuously]
Nachimuthu S, Assar MD, Schussler JM. Drug-induced QT interval prolongation: mechanisms and clinical management. Ther Adv Drug Saf. 2012;3(5):241–253.
Roden DM. Drug-Induced Prolongation of the QT Interval. N Engl J Med. 2004;350:1013–1022.
Drew BJ, et al. Prevention of Torsade de Pointes in Hospital Settings: A Scientific Statement From the American Heart Association and the American College of Cardiology Foundation. Circulation. 2010;121:1047–1060.

Refill Calendar

Tools for tracking controlled and restricted medication fills — days between dates, usage analysis, and refill date projection.

📅 Days Between Two Dates

Calculate the exact number of days between any two dates.

First Date

Second Date

⚙ Usage Calculator

Estimate average daily use, monthly consumption, and percentage over- or underuse compared to the prescribed regimen.

Fill Date

End / Count Date

Pills Prescribed

Pill Strength

Unit

Prescribed pills/day

Pills remaining at count (optional)

▶ Forward Refill Dates

Enter a fill date and days supply to project the next 6 refill dates.

Fill Date

Days Supply

◀ Reverse Refill Tracker

Enter the most recent fill date and expected days between fills to estimate when the previous 6 fills should have occurred.

Most Recent Fill Date

Days Between Fills

🔄 Medication Sync

Align two medications to a common refill date using a one-time short fill. Enter each medication's last fill date, days supply, quantity dispensed, and daily dose.

Medication A

Name (optional)

Last Fill Date

Days Supply

Qty Dispensed

Daily Dose (units/day)

Medication B

Name (optional)

Last Fill Date

Days Supply

Qty Dispensed

Daily Dose (units/day)

Preferred Sync Date (optional)Leave blank to auto-align to the latest depletion date

Future Fills to Show

Cognitive Domains

Cognitive domains, standardized screening instruments, and clinical interpretation.

🧠 Overview of Cognitive Domains

Cognitive functioning is organized into hierarchical domains. Lower-order domains involve basic sensory and motor processing; higher-order domains involve reasoning, memory, and executive control. Impairments rarely occur in isolation — executive functioning, at the top of the hierarchy, depends on the integrity of every domain below it.

7 Executive Functioning Top-Down Control

6 Processing Speed Cross-Domain

5 Language & Verbal Skills Temporal / Frontal

4 Memory Hippocampus / Frontal

3 Attention & Concentration Frontal / Parietal

2 Motor Skills & Construction Frontal / Parietal

1 Sensation & Perception Primary Cortex

Domain conceptualization follows Harvey PD. Dialogues Clin Neurosci. 2019;21(3):227–237. Domain numbering reflects bottom-up hierarchy (1 = most basic).

7

Executive Functioning

Reasoning • Problem Solving • Cognitive Flexibility

The top-down set of processes that coordinate and control all other cognitive domains. Includes planning, abstract reasoning, impulse inhibition, and the ability to shift strategies in response to feedback. Requires intactness of every lower domain. Classical tests include the Wisconsin Card Sorting Test (WCST). Perseverative errors — repeating a response strategy already known to be incorrect — are a hallmark failure.

Subdomains: Reasoning, problem solving, cognitive flexibility, inhibition/response management, prospective memory (planning component)

MoCA

Trail Making (1→A→2→B…) — alternating sequence tests set-shifting 1 pt
Clock drawing — planning and organization 3 pts
Abstraction (train–bicycle; ruler–watch) — conceptual reasoning 2 pts
Serial 7s — sustained calculation/mental control 3 pts

SLUMS

Math word problem ($100 − $3 − $20) — calculation and reasoning 3 pts
Clock drawing — planning and visuospatial organization 4 pts
Story recall involves narrative organization strategy 8 pts

Impaired in: Schizophrenia (problem-solving, organization), ADHD (impulsivity, inattention), OCD (inefficient processing), depression, frontostriatal degenerative conditions, TBI.

6

Processing Speed

Speed of Cognitive Operations

The rate at which cognitive tasks are performed. Often the most impaired domain in schizophrenia and most strongly correlated with functional impairment. Processing speed affects performance on "non-speeded" tasks as well, since even list learning presents stimuli at a fixed rate. Prototypical tasks include Symbol Coding and Trail Making Part A.

Subdomains: Coding and tracking speed, semantically relevant speed (verbal fluency), psychomotor speed

MoCA

Verbal fluency (F words, 1 min) — timed output reflects processing speed 1 pt
Trail Making has implicit speed demand in clinical use
Note: MoCA does not include a dedicated processing speed task

SLUMS

Animal fluency (1 min) — timed semantic retrieval reflects processing speed 3 pts
Note: SLUMS does not include a dedicated processing speed task

Impaired in: Schizophrenia (most impaired domain), major depression, Parkinson's disease, frontostriatal degenerative conditions. Less affected by normal aging than working memory.

5

Language & Verbal Skills

Naming • Fluency • Comprehension

Includes both receptive and expressive language: understanding instructions, accessing semantic memory to name objects, and generating verbal output. Fluency tasks require naming as many members of a category (or letter) as possible in one minute. Naming deficits (anomia) are more characteristic of cortical dementia (Alzheimer's) than frontostriatal conditions.

Subdomains: Object naming, verbal fluency (letter/category), sentence repetition, reading comprehension, semantic access

MoCA

Animal naming — 3 pictures (lion, rhino, camel) 3 pts
Sentence repetition — 2 sentences, exact repetition required 2 pts
Verbal fluency — words beginning with F, ≥11 words = 1 pt 1 pt

SLUMS

Animal fluency — category (animals, 1 min): 0–4 = 0pt, 5–9 = 1pt, 10–14 = 2pt, 15+ = 3pt 3 pts

Impaired in: Alzheimer's disease (naming > fluency), frontostriatal dementia (fluency more than naming), stroke/aphasia, schizophrenia (executive access to semantic storage).

4

Memory

Working • Episodic • Semantic • Prospective

The most complex and multifaceted cognitive domain. Working memory holds information in consciousness for immediate use (maintenance) and operates on it (manipulation). Episodic memory involves encoding, storing, and retrieving personally experienced events. Distinguishing encoding failure from retrieval failure is clinically important: retrieval failure improves with cueing; encoding failure does not. Semantic memory stores general world knowledge and is relatively preserved in aging. Prospective memory — remembering to carry out future intentions — is implicated in medication adherence.

Subdomains: Working memory (maintenance / manipulation), episodic memory (encoding / storage / retrieval), semantic memory, procedural memory, prospective memory

MoCA

Forward digit span 2-1-8-5-4 — working memory maintenance 1 pt
Backward digit span 7-4-2 — working memory manipulation 1 pt
Word list (FACE, VELVET, CHURCH, DAISY, RED) × 2 trials — encoding; no points 0 pts
Delayed free recall (5 words after ~5 min) — episodic retrieval 5 pts
Memory Index Score (MIS) — distinguishes retrieval vs encoding failure (category cues × 2, forced-choice × 1) sub-score /15
Orientation (date, month, year, day, place, city) — semantic/temporal orientation 6 pts

SLUMS

Orientation: day, year, state 3 pts
5 objects encoding (Apple, Pen, Tie, House, Car) — no points for encoding 0 pts
5 objects recall — episodic retrieval 5 pts
Digit span backwards (87 → 78; 648 → 846; 8537 → 7358) — working memory manipulation 2 pts
Story recall (Jill the stockbroker) — narrative episodic memory (4 questions × 2 pts) 8 pts

Impaired in: Alzheimer's disease (encoding + delayed recall + recognition all impaired), frontostriatal dementia (encoding + recall impaired, but recognition/cued recall often spared), schizophrenia (episodic + prospective memory), normal aging (working memory, processing-speed-dependent tasks).

3

Attention & Concentration

Selective • Sustained • Divided

Selective attention is the ability to attend to relevant information while ignoring distractors. Sustained attention (vigilance) refers to maintaining detection over time — classically assessed with the Continuous Performance Test (CPT), where the patient taps on a specific target letter in a stream. Errors of omission (missing targets) are common in psychosis; errors of commission (false positives) predominate in ADHD. Divided/dual-task attention requires processing two information streams simultaneously and becomes automated with practice.

Subdomains: Selective attention, sustained attention/vigilance, divided attention, dual-task processing, response inhibition

MoCA

Letter A vigilance (tap at each A in letter stream) — sustained attention, CPT analog 1 pt
Serial 7s (100−7 five times) — focused concentration, resistance to interference 3 pts

SLUMS

Shape identification (place X in triangle; identify largest figure) — selective visual attention 2 pts
Math word problem requires sustained attention to multi-step instructions 3 pts

Impaired in: ADHD (commission errors, impulsivity), schizophrenia (omission errors, reduced d′), TBI, delirium, severe anxiety. Dual-task processing especially impaired in schizophrenia spectrum.

2

Motor Skills & Construction

Fine Motor • Copying • Drawing

Motor skills encompass fine motor dexterity, speed, reaction time, and grip strength — assessable with finger tapping, pegboard tasks, and grip dynamometry. These have minimal cognitive demands and help identify lateralized dysfunction. Construction is the ability to copy or produce drawings of objects. The clock drawing task is particularly rich — it engages construction, planning (executive), and visual attention simultaneously. Construction deficits are commonly found in dementia and right parietal lesions.

Subdomains: Fine motor speed, manual dexterity, reaction time, visual construction (copying, drawing), praxis

MoCA

Copy cube — 3D spatial construction 1 pt
Clock drawing (contour, numbers, hands at 10 past 11) — visuospatial construction + executive planning 3 pts

SLUMS

Clock drawing (hour markers + time at 10 min to 11) — visuospatial construction 4 pts
Place X in triangle — visual-spatial accuracy, basic praxis 1 pt
Identify largest figure — visual discrimination 1 pt

Impaired in: Right parietal lesions (construction deficits, neglect), Alzheimer's disease, Parkinson's disease (motor slowing), DLB, parietal strokes, normal aging (fine motor slowing).

1

Sensation & Perception

Sensory Detection • Object Recognition

Sensation is the detection of stimuli across the five sensory modalities. Perception involves integrating and recognizing sensory input — identifying previously experienced objects, sounds, smells, and spatial orientations. Agnosia is the inability to recognize previously identifiable stimuli despite intact primary sensation and is modality-specific. Neglect — inattention to a full hemifield — is a perceptual deficit seen after right-hemisphere stroke.

Subdomains: Visual/auditory/tactile/olfactory acuity, object recognition, spatial orientation, multisensory integration

MoCA

Animal naming images (lion, rhino, camel) — involves visual perception + semantic retrieval 3 pts (overlaps Language)
No dedicated primary sensation/perception items — assumes intact basic senses

SLUMS

Shape identification and size discrimination — basic visual perception 2 pts (overlaps Attention)
Neither screen assesses primary sensation — clinical exam or specialized testing required

Impaired in: Right parietal strokes (contralateral neglect, visuospatial agnosia), occipital lesions (visual agnosia), temporal lesions (auditory agnosia, prosopagnosia), Lewy body dementia (early visuoperceptual deficits).

📋 MoCA vs. SLUMS — Domain Coverage Comparison

Both tests assess 30 total points. Coverage of cognitive domains differs; combined use provides broader sampling. Training and certification are required to administer and interpret the MoCA.

Cognitive Domain	MoCA Task(s)	MoCA Pts	SLUMS Task(s)	SLUMS Pts
Executive	Trail Making (alternating), Clock (planning), Abstraction, Serial 7s	9	Math word problem, Clock (planning), Story (organization)	15*
Processing Speed	Verbal fluency (F words, timed)	1	Animal fluency (timed)	3
Language	Naming (3 animals), Sentence repetition (×2), Verbal fluency	6	Animal fluency	3
Memory	Forward/backward digit span, Word encoding (×2), Delayed recall, MIS, Orientation	13	Orientation (×3), 5-object recall, Digit span backwards, Story recall	18
Attention	Letter A vigilance, Serial 7s	4	Shape identification, Math problem (multi-step)	5*
Motor / Construction	Copy cube, Clock drawing	4	Clock drawing, X in triangle, Largest figure	6
Sensation / Perception	Neither screen directly assesses primary sensation/perception — assumes intact basic senses. Perceptual items overlap with Language (naming) and Attention (shape).

* Domain points overlap; individual tasks often engage multiple domains simultaneously. Point values reflect primary domain attribution.

🎯 Score Interpretation

Montreal Cognitive Assessment (MoCA) — 30 Points

+1 point if ≤12 years formal education (max 30). Administration ~10 minutes. Normal ≥26/30. Training and certification required for clinical interpretation (www.mocatest.org).

26–30

Normal Cognition

18–25

Mild Cognitive Impairment

10–17

Moderate Impairment

<10

Severe Impairment

MoCA sensitivity for MCI ~90%; specificity ~87% (Nasreddine et al., J Am Geriatr Soc, 2005). A score below 26 does not automatically indicate dementia; scores must be interpreted alongside clinical history, education, and medical evaluation. A score ≥26 after a dementia diagnosis does not indicate resolution.

Saint Louis University Mental Status Exam (SLUMS) — 30 Points

Validated for detection of mild neurocognitive disorder and dementia. Scoring varies by education level. No certification required. May be more sensitive than MMSE for mild impairment.

High School Education

27–30

Normal

21–26

Mild Neurocognitive Disorder

1–20

Dementia

Less than High School Education

25–30

Normal

20–24

Mild Neurocognitive Disorder

1–19

Dementia

Tariq SH, et al. Am J Geriatr Psych. 2006;14:900–910. SLUMS may be more sensitive than MMSE for detecting MCI. Education-adjusted scoring is essential. Scores are one tool among many — full clinical evaluation including history, collateral information, neuroimaging, and laboratory workup is required for diagnosis.

Classic Neuropsychiatric Circuits

Parallel cortico–basal ganglia–thalamo–cortical loops and limbic circuits.

🧠 Classic Neuropsychiatric Circuits

Several circuits are repeatedly referenced in neuropsychiatry because they link brain anatomy to cognition, behavior, and psychiatric symptoms. Most originate from Alexander, DeLong & Strick's landmark 1986 description of parallel cortico–basal ganglia–thalamo–cortical loops, each specialized for a distinct functional domain.

The Parallel Loop Framework Alexander, DeLong & Strick, 1986

Dorsolateral Prefrontal Executive Function / Cognition

Orbitofrontal Behavioral Inhibition / Impulse Control

Anterior Cingulate Motivation / Effort Allocation

Motor Movement Initiation & Control

All four loops share the same basic architecture: Cortex → Striatum → Globus Pallidus/SNr → Thalamus → Cortex. What differs is which cortical region anchors the loop and therefore which function is modulated. This framework underlies DBS target selection, neuropsychiatric differential diagnosis, and neuroimaging interpretation.

🧠 Explore in 3D →DLPFC OFC/vmPFC ACC Striatum MD thalamus NAcc VTA/SNc Open Explorer ↗

◌ Cortico–Basal Ganglia–Thalamo–Cortical Loops Alexander, DeLong & Strick, 1986 · Tekin & Cummings, 2002

1

Dorsolateral Prefrontal Circuit

Executive Circuit • Cognitive Control Loop

Cortico-BG Loop

DLPFC

→

Caudate Nucleus

→

Globus Pallidus / SNr

→

Thalamus (VA/MD)

↩ back to DLPFC

Functions

Executive function & cognitive control
Working memory (maintenance + manipulation)
Planning and goal-directed behavior
Cognitive flexibility / set-shifting
Problem solving

Clinical Associations

Schizophrenia hypofrontality ADHD Major Depressive Disorder Frontotemporal Dementia TBI

Dysfunction presents as: Poor organization Impaired working memory Reduced problem solving Cognitive slowing Perseveration

2

Orbitofrontal Circuit

Behavioral Inhibition Circuit • Impulse Control Loop

Cortico-BG Loop

Orbitofrontal Cortex

→

Ventromedial Caudate

→

Globus Pallidus / SNr

→

Thalamus (VA/MD)

↩ back to OFC

Functions

Impulse control and behavioral inhibition
Social judgment and contextual behavior
Reward evaluation and value-based decision making
Emotional regulation via prefrontal modulation

Clinical Associations

OCD hyperactivation of loop Tourette Syndrome Frontotemporal Dementia Substance Use Disorder

Dysfunction presents as: Disinhibition Impulsivity Socially inappropriate behavior Compulsivity Poor reward prediction

3

Anterior Cingulate Circuit

Motivation / Apathy Circuit • Effort Allocation Loop

Cortico-BG Loop

Anterior Cingulate Cortex

→

Ventral Striatum (NAc)

→

Ventral Pallidum

→

Thalamus (MD)

↩ back to ACC

Functions

Motivation and initiation of behavior
Effort allocation toward goals
Emotional processing and salience detection
Error monitoring and response conflict

Clinical Associations

Major Depressive Disorder apathy, anhedonia Parkinson Disease TBI akinetic mutism Apathy syndromes

Dysfunction presents as: Apathy Reduced initiative Loss of motivation Mutism (extreme) Anhedonia

◈ Limbic Circuits Papez, 1937 · LeDoux, 2003

4

Papez Circuit

Emotion & Memory Circuit • Originally described by James Papez, 1937

Limbic

Hippocampus

→

Fornix

→

Mammillary Bodies

→

Anterior Thalamus

→

Cingulate Gyrus

↩ back to Hippocampus

Functions

Emotional processing and subjective emotional experience
Episodic memory encoding and consolidation
Integration of emotional context with memory
Spatial navigation (hippocampal component)

Clinical Associations

Alzheimer Disease hippocampal atrophy Korsakoff Syndrome mammillary body lesion Temporal Lobe Epilepsy TBI fornix disruption

Dysfunction presents as: Anterograde amnesia Emotional blunting Confabulation Impaired episodic recall

5

Amygdala–Prefrontal Circuit

Fear & Salience Circuit • Threat Detection Loop

Limbic

Amygdala

⇄

Ventromedial PFC

⇄

Hippocampus

(bidirectional regulation; vmPFC inhibits amygdala)

Functions

Fear acquisition and extinction learning
Threat detection and emotional salience
Contextual modulation of fear (vmPFC)
Conditioned fear responses

Clinical Associations

PTSD amygdala hyperactivity, vmPFC hypo Panic Disorder Generalized Anxiety Disorder Social Anxiety Disorder

Dysfunction presents as: Hypervigilance Exaggerated startle Intrusive fear memories Impaired extinction Avoidance

◆ Dopamine Projection Circuits Schultz, 1998 · Stahl, 2021

6

Mesolimbic Dopamine Circuit

Reward & Reinforcement Circuit • VTA → NAc Pathway

Dopamine

VTA

→

Nucleus Accumbens

→

Limbic Structures

(amygdala, hippocampus, prefrontal cortex)

Functions

Reward processing and hedonic response
Motivation and incentive salience
Reinforcement learning (prediction error signal)
Drug-induced euphoria and craving

Clinical Associations

Schizophrenia positive symptoms: ↑DA Addiction / SUD dopamine dysregulation MDD anhedonia: ↓DA signaling Bipolar Disorder mania: ↑DA

Dysfunction presents as: Anhedonia (↓DA) Psychosis — positive sx (↑DA) Drug craving Impaired reward learning

Pharmacological relevance: Antipsychotics block D₂ receptors in this pathway — responsible for both therapeutic reduction of positive symptoms and risk of EPS at higher doses. Psychostimulants (cocaine, amphetamines) flood this circuit with dopamine.

7

Mesocortical Dopamine Circuit

Cognitive Dopamine Circuit • VTA → PFC Pathway

Dopamine

VTA

→

Prefrontal Cortex

→

Limbic & Striatal Areas

(modulates DLPFC and ACC circuits)

Functions

Executive function and working memory (D1 receptors on PFC)
Motivation and effort-based decision making
Cognitive aspects of goal-directed behavior
Modulates DLPFC and ACC loop activity

Clinical Associations

Schizophrenia negative/cognitive sx: ↓DA in PFC ADHD ↓DA/NE in PFC MDD cognitive symptoms

Dysfunction presents as: Negative symptoms (schiz.) Cognitive deficits Poor working memory Amotivation

Pharmacological relevance: An inverted-U relationship exists between dopamine tone and PFC function — too little (schizophrenia negative symptoms) or too much (stimulant excess) both impair cognition. ADHD medications (methylphenidate, amphetamines) boost DA/NE in PFC. Antipsychotic D₂ blockade in this circuit may worsen negative symptoms and cognition.

▸ Motor Circuit DeLong, 1990 · often co-taught with psychiatric loops

8

Motor Basal Ganglia Circuit

Movement Initiation Loop • Included as the structural template for all loops

Motor

Motor Cortex (M1/SMA)

→

Putamen

→

GPi / SNr

→

Thalamus (VL/VA)

↩ back to Motor Cortex

Functions

Initiation and scaling of voluntary movement
Selection of appropriate motor programs
Suppression of competing/unwanted movements
Template architecture for all parallel BG loops

Clinical Associations

Parkinson Disease ↓DA in putamen → GPi disinhibition Huntington Disease striatal neurodegeneration Tardive Dyskinesia D₂ blockade supersensitivity Tourette Syndrome striatal overactivity

Dysfunction presents as: Bradykinesia (↓DA) Rigidity Chorea / tics (striatal loss) Tremor Tardive dyskinesia

Pharmacological relevance: Antipsychotic D₂ blockade in the putamen produces parkinsonian EPS. Antiparkinsonian agents (levodopa, DA agonists) restore dopamine tone. DBS of the STN or GPi targets this circuit. Understanding direct vs. indirect pathways (striatum → GPi vs. striatum → GPe → STN → GPi) explains both the physiology and pharmacology of movement disorders.

⚡ Quick Clinical Heuristic — Symptom to Circuit

When a patient presents with a neuropsychiatric symptom cluster, this mapping provides a starting point for circuit-level localization. Symptoms rarely reflect a single circuit; overlap is the rule.

Symptom / Presentation	Primary Circuit	Key Neurotransmitter	Example Conditions
Executive dysfunction, poor planning	DLPFC Circuit	Dopamine (D1, PFC)	Schizophrenia, ADHD, MDD, FTD
Impulsivity, disinhibition, compulsions	Orbitofrontal Circuit	Serotonin, Dopamine	OCD, Tourette, FTD, SUD
Apathy, amotivation, anhedonia	Anterior Cingulate Circuit	Dopamine (mesolimbic)	MDD, Parkinson, TBI
Anxiety, fear, hypervigilance	Amygdala–PFC Circuit	GABA, Serotonin, NE	PTSD, GAD, Panic Disorder
Positive psychotic symptoms (hallucinations, delusions)	Mesolimbic Circuit	Dopamine (↑D2, NAc)	Schizophrenia, mania, stimulant psychosis
Negative / cognitive symptoms	Mesocortical Circuit	Dopamine (↓D1, PFC)	Schizophrenia, ADHD, MDD
Memory impairment	Papez Circuit	ACh, Glutamate	Alzheimer, Korsakoff, TBI
Movement disorder (rigidity, chorea, tics)	Motor BG Circuit	Dopamine (putamen)	Parkinson, Huntington, Tourette, TD

Brain Regions in Neuropsychiatric Disorders

Neuroanatomical correlates of major psychiatric and neurological diagnoses.

🧠 Brain Regions in Neuropsychiatric Disorders

Each major neuropsychiatric condition is associated with dysfunction in a characteristic set of brain regions. Region involvement is based on convergent evidence from structural MRI, functional neuroimaging, lesion studies, and postmortem data. Colors indicate brain region category.

Prefrontal / Frontal Cortex Cingulate Cortex Amygdala Hippocampus / MTL Striatum / Basal Ganglia Thalamus Temporal Cortex Cerebellum Brainstem / SN Insula / Parietal

🧠 Explore in 3D →DLPFC ACC Amygdala Hippocampus Striatum MD thalamus NAcc VTA/SNc Open Explorer ↗

■ Anxiety & Trauma Disorders Amygdala-PFC circuit • Fear / threat network

Post-Traumatic Stress Disorder

PTSD

Amygdala Hippocampus Ventromedial PFC Anterior Cingulate

Hyperactivation of the amygdala drives exaggerated fear responses and intrusive memories. The vmPFC normally suppresses amygdala activation during extinction — this inhibition is impaired in PTSD. Hippocampal volume reduction contributes to impaired contextual fear memory, resulting in generalized (context-independent) fear responses.

Fear learning & impaired extinction Hypervigilance Intrusive memories Avoidance

→ Circuit: Amygdala–PFC Circuit (#5)

Generalized Anxiety Disorder

GAD

Amygdala Bed Nucleus of Stria Terminalis Insula Prefrontal Cortex

Unlike PTSD (cue-dependent fear), GAD involves sustained, diffuse apprehension mediated by the bed nucleus of the stria terminalis (BNST) — a structure implicated in anticipatory anxiety. The insula processes interoceptive signals contributing to somatic anxiety symptoms. Prefrontal hypoactivation impairs top-down regulation of the threat network.

Sustained threat monitoring Interoceptive hyperawareness Anticipatory anxiety

→ Circuit: Amygdala–PFC Circuit (#5)

■ OCD & Related Disorders Orbitofrontal circuit • Cortico-striatal hyperactivation

Obsessive-Compulsive Disorder

OCD

Orbitofrontal Cortex Caudate Nucleus Anterior Cingulate Thalamus

OCD is characterized by hyperactivation of the orbitofrontal–caudate–thalamic loop. Normally the OFC evaluates action outcomes and the caudate gates habitual behaviors — in OCD this loop becomes "stuck," generating repetitive, compulsive thoughts and behaviors. Neuroimaging consistently shows increased activity in the OFC and caudate at rest, normalizing with successful treatment (SSRIs or CBT).

Cortico-striatal loop hyperactivation Behavioral inhibition failure Error monitoring excess

→ Circuit: Orbitofrontal Circuit (#2)

Tourette Syndrome

TS

Striatum (Caudate + Putamen) Orbitofrontal Cortex Supplementary Motor Area Thalamus

Tourette syndrome involves hyperactivation of cortico-striatal sensorimotor loops, generating premonitory urges and tics. Striatal overactivity releases suppressed motor programs, producing involuntary vocalizations and movements. High comorbidity with OCD (same orbitofrontal loop) and ADHD (same frontostriatal network) reflects shared circuit overlap.

Striatal motor hyperactivation Impaired tic suppression Premonitory urges

→ Circuit: Orbitofrontal + Motor Circuits (#2, #8)

■ Mood Disorders Anterior cingulate • Subgenual network • Limbic-cortical model

Major Depressive Disorder

MDD

Subgenual ACC (sgACC / Area 25) Ventromedial PFC Hippocampus Amygdala Nucleus Accumbens

Mayberg's limbic-cortical model describes MDD as hyperactivity of the subgenual ACC (sgACC/Area 25) driving sustained negative affect, while the dorsal PFC is hypoactive (impairing cognitive regulation). Hippocampal volume loss — partially reversible with antidepressants and exercise — reflects glucocorticoid toxicity from chronic stress. Nucleus accumbens hypoactivation underlies anhedonia. The sgACC is the primary target of deep brain stimulation for treatment-resistant depression.

Limbic-cortical dysregulation Anhedonia (NAc/reward) Hippocampal neuroplasticity Negative cognitive bias

→ Circuits: Anterior Cingulate (#3) • Mesolimbic (#6)

Bipolar Disorder

BD

Amygdala Ventrolateral PFC Anterior Cingulate Ventral Striatum

Bipolar disorder is associated with amygdala hyperactivity and insufficient prefrontal regulation across mood states. The ventrolateral PFC, which normally modulates emotional responses, shows structural and functional abnormalities. Ventral striatum dysregulation drives the elevated reward sensitivity and impulsivity of manic episodes. Amygdala volume enlargement (opposite to MDD's reduction) is among the most replicated findings.

Emotional dysregulation Reward hypersensitivity (mania) Prefrontal-limbic imbalance

→ Circuits: Anterior Cingulate (#3) • Mesolimbic (#6)

■ Psychotic Disorders Dopamine dysregulation • DLPFC hypofrontality • Thalamic gating

Schizophrenia

SCZ

Dorsolateral PFC Hippocampus Thalamus Striatum Superior Temporal Cortex

Schizophrenia involves a complex interaction between hypofrontality (↓dopamine in DLPFC → negative/cognitive symptoms) and mesolimbic hyperdopaminergia (↑dopamine in striatum → positive symptoms). The thalamus acts as a sensory gating mechanism; thalamic abnormalities may explain the flooding of consciousness with irrelevant stimuli that contributes to psychosis. Superior temporal cortex (including Wernicke's area) volume loss correlates with auditory hallucinations. Hippocampal hyperactivation disrupts pattern completion and separation, potentially driving the associative loosening and false inference seen in delusions.

Hypofrontality (negative/cognitive sx) Mesolimbic ↑DA (positive sx) Thalamic gating failure Auditory hallucinations (temporal)

DA imbalance model: The same D₂ receptor — blocked by antipsychotics — produces therapeutic effects in the striatum (reducing positive symptoms) but worsens function in the DLPFC (worsening negative/cognitive symptoms). This is why antipsychotics treat psychosis but often do not improve — and may worsen — cognition.

→ Circuits: DLPFC (#1) • Mesolimbic (#6) • Mesocortical (#7)

■ Neurodevelopmental Disorders Fronto-striatal attention • Social brain network • Connectivity differences

ADHD

Dorsolateral PFC Anterior Cingulate Caudate & Putamen Cerebellum

ADHD is a disorder of fronto-striatal attention and executive networks. The DLPFC and ACC are hypoactive, impairing working memory, planning, and error monitoring. Reduced dopaminergic and noradrenergic tone in the PFC is the primary target of stimulant therapy. Caudate volume reduction (which normalizes with stimulant treatment) reflects delayed neural maturation rather than fixed damage. The cerebellum contributes to timing deficits and cognitive coordination.

Frontostriatal underactivation ↓DA/NE in PFC Delayed cortical maturation Motor/timing imprecision

Shared BG circuitry with OCD and Parkinson: All three involve basal ganglia dysfunction, but in distinct ways — ADHD shows underactive fronto-striatal signaling, OCD shows hyperactive orbitofrontal loop, and Parkinson shows dopamine depletion in the motor putamen. This explains why dopamine-modulating drugs influence all three.

→ Circuits: DLPFC (#1) • Anterior Cingulate (#3) • Mesocortical (#7)

Autism Spectrum Disorder

ASD

Superior Temporal Sulcus Amygdala Fusiform Gyrus Medial PFC Cerebellum

Autism involves differences in three interconnected systems: the social brain network (STS, fusiform face area, amygdala, mPFC — involved in face recognition, social perception, and theory of mind), long-range connectivity (frequently underconnected between distant regions, overconnected locally), and cerebellar circuits (affecting timing of social responses, motor coordination, and predictive processing). Amygdala differences contribute to atypical salience assignment to social stimuli.

Social perception differences Face recognition (fusiform) Altered connectivity patterns Predictive processing (cerebellum)

Connectivity model: Rather than focal lesions, ASD is increasingly conceptualized as a disorder of connectivity — long-range underconnection (reducing integration across brain networks) alongside local overconnection (producing sensory hypersensitivity and restricted processing patterns).

→ Network: Social Brain Network • Default Mode Network

■ Neurodegenerative Disorders Progressive structural loss • Network degeneration

Alzheimer Disease

AD

Hippocampus Entorhinal Cortex Temporal Cortex Posterior Cingulate / PCC

Alzheimer pathology (amyloid plaques and tau neurofibrillary tangles) spreads in a stereotyped pattern described by Braak staging: beginning in the entorhinal cortex and hippocampus (explaining early episodic memory loss), progressing to temporal and parietal association cortices, then frontal lobes. The posterior cingulate and precuneus — hubs of the default mode network — show early hypometabolism on FDG-PET, making them important imaging biomarkers. Cholinergic depletion from the basal forebrain (nucleus basalis of Meynert) is the pharmacological target of acetylcholinesterase inhibitors.

Episodic memory loss (hippocampus) Braak staging (entorhinal → cortex) Default mode network hypometabolism Cholinergic deficit (nbM)

→ Circuit: Papez Circuit (#4)

Parkinson Disease

PD

Substantia Nigra (pars compacta) Putamen (Basal Ganglia) Motor Cortex Locus Coeruleus

Parkinson disease results from progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc), depleting dopamine in the putamen and disrupting the motor basal ganglia circuit. Loss of the direct pathway's activation and overactivation of the indirect pathway → increased GPi inhibition of thalamus → reduced cortical motor output (bradykinesia, rigidity). Braak's staging of Parkinson pathology suggests it begins in the brainstem (locus coeruleus, dorsal vagal nucleus) before reaching the SNpc, explaining non-motor prodromal symptoms (REM sleep disorder, anosmia, constipation).

SNpc dopamine depletion Direct/indirect pathway imbalance Bradykinesia, rigidity, tremor Braak staging (brainstem → cortex)

→ Circuit: Motor BG Circuit (#8)

Frontotemporal Dementia

FTD

Frontal Lobes (bilateral) Anterior Temporal Lobes Anterior Cingulate Orbitofrontal Cortex

FTD involves selective degeneration of the frontal and anterior temporal lobes, with relative sparing of posterior regions (distinguishing it from Alzheimer). The behavioral variant (bvFTD) causes disinhibition, apathy, and social inappropriateness — reflecting orbitofrontal and anterior cingulate degeneration. Primary progressive aphasias (semantic dementia, PNFA) reflect asymmetric temporal or frontal language network loss. Unlike Alzheimer, episodic memory is often relatively preserved early; executive function and behavior are the first casualties.

Behavioral disinhibition (OFC loss) Apathy (ACC degeneration) Social inappropriateness Language (PPA variants)

→ Circuits: Orbitofrontal (#2) • Anterior Cingulate (#3) • DLPFC (#1)

■ Alcohol-Related & Nutritional Disorders Papez circuit • Thiamine-dependent injury • Frontal degeneration

Wernicke Encephalopathy

WE

Mammillary Bodies Thalamus (medial) Periaqueductal Gray Cerebellum

Wernicke encephalopathy results from acute thiamine (B₁) deficiency, causing hemorrhagic necrosis in thiamine-dependent high-metabolic regions. The classic triad: ophthalmoplegia (periaqueductal gray/oculomotor nuclei), ataxia (cerebellum), and confusion/encephalopathy (thalamic and mammillary body involvement). MRI shows characteristic T2/FLAIR hyperintensity around the aqueduct and in medial thalami. Treatment must not be delayed — thiamine must precede glucose in suspected cases. Untreated, it progresses to Korsakoff syndrome.

Acute thiamine deficiency Ophthalmoplegia (PAG) Ataxia (cerebellum) Encephalopathy (thalamus)

→ Progresses to: Korsakoff Syndrome if untreated

Korsakoff Syndrome

KS

Mammillary Bodies Medial Thalamus (MD nucleus) Hippocampus

The chronic amnestic syndrome following Wernicke encephalopathy. Bilateral mammillary body atrophy and mediodorsal thalamic lesions disrupt the Papez circuit, resulting in profound anterograde amnesia (inability to form new memories) with relatively preserved remote memory, procedural learning, and intellectual function. Confabulation — producing false memories without intent to deceive — is a characteristic feature, reflecting disinhibited memory retrieval processes. The MD thalamic nuclei serve as a relay between frontal lobes and hippocampus; their damage disrupts frontal monitoring of memory output.

Anterograde amnesia Confabulation Papez circuit disruption Procedural memory preserved

→ Circuit: Papez Circuit (#4)

Alcohol-Related Brain Damage

ARBD

Frontal Lobes Cerebellum Corpus Callosum Hippocampus

Chronic alcohol exposure causes direct neurotoxicity (ethanol and acetaldehyde), thiamine deficiency, glutamate excitotoxicity during repeated withdrawals, and oxidative stress. The frontal lobes — responsible for executive function — are disproportionately vulnerable, producing disinhibition, poor planning, and impulsivity. Cerebellar degeneration causes persistent ataxia. Corpus callosum demyelination (Marchiafava-Bignami disease in severe cases) disrupts inter-hemispheric communication. Unlike Korsakoff, ARBD involves broader, more diffuse damage with potential for partial recovery with abstinence.

Executive dysfunction (frontal) Ataxia (cerebellum) Callosal demyelination Partial reversibility with abstinence

→ Circuits: DLPFC (#1) • Motor (#8)

📈 Network → Disorder Quick Reference

Network / Circuit	Primary Disorders	Key Brain Regions
Amygdala Fear Network	PTSD, GAD, Panic Disorder	Amygdala, vmPFC, hippocampus, BNST
Orbitofrontal Loop	OCD, Tourette, FTD (behavioral)	OFC, caudate, thalamus, ACC
Frontostriatal Attention Network	ADHD, Schizophrenia (cognitive), MDD	DLPFC, caudate/putamen, ACC, cerebellum
Subgenual / Mood Network	MDD, Bipolar Disorder	sgACC, vmPFC, amygdala, NAc
Reward Network (Striatum)	Bipolar (mania), Addiction, MDD (anhedonia)	NAc, VTA, OFC, ventral striatum
DLPFC Cognitive Network	Schizophrenia (negative/cognitive), ADHD	DLPFC, thalamus, dorsal striatum
Memory Network (Hippocampus)	Alzheimer, Korsakoff, PTSD	Hippocampus, entorhinal cx, mammillary bodies, thalamus
Social Brain Network	ASD, Social Anxiety Disorder	STS, fusiform, amygdala, mPFC
Nigrostriatal Motor Network	Parkinson, Huntington, Tardive Dyskinesia	SNpc, putamen, GPi, motor cortex

📚 References

Harvey PD. Domains of cognition and their assessment. Dialogues Clin Neurosci. 2019;21(3):227–237.
Nasreddine ZS, Phillips NA, Bédirian V, et al. The Montreal Cognitive Assessment, MoCA: a brief screening tool for mild cognitive impairment. J Am Geriatr Soc. 2005;53(4):695–699.
Tariq SH, Tumosa N, Chibnall JT, et al. The Saint Louis University Mental Status (SLUMS) examination. Am J Geriatr Psych. 2006;14:900–910.
Lezak MD, Howieson DB, Bigler ED, Tranel D. Neuropsychological Assessment. 5th ed. Oxford University Press; 2012.
Folstein MF, Folstein SE, McHugh PR. Mini-Mental State. J Psychiatr Res. 1975;12:189–198.
Paulsen JS, Salmon DP, Monsch A, et al. Discrimination of cortical from subcortical dementias. J Clin Psychol. 1995;51:48–58.
Twamley EW, et al. Prospective memory impairment in schizophrenia. Schizophr Res. 2007;106:42–49.
Alexander GE, DeLong MR, Strick PL. Parallel organization of functionally segregated circuits linking basal ganglia and cortex. Annu Rev Neurosci. 1986;9:357–381.
Tekin S, Cummings JL. Frontal-subcortical neuronal circuits and clinical neuropsychiatry: an update. J Psychosom Res. 2002;53(2):647–654.
Papez JW. A proposed mechanism of emotion. Arch Neurol Psychiatry. 1937;38(4):725–743.
LeDoux JE. The emotional brain, fear, and the amygdala. Cell Mol Neurobiol. 2003;23(4–5):727–738.
Schultz W. Predictive reward signal of dopamine neurons. J Neurophysiol. 1998;80(1):1–27.
Haber SN. Corticostriatal circuitry. Dialogues Clin Neurosci. 2016;18(1):7–21.
Cummings JL, Mega MS. Neuropsychiatry and Behavioral Neuroscience. Oxford University Press; 2003.
Stahl SM. Stahl's Essential Psychopharmacology. 5th ed. Cambridge University Press; 2021.

3D Brain Explorer

Interactive, expert-segmented 3D neuroanatomy for the structures that matter in psychopharmacology. Click a structure to see its role and jump to the related circuit or region.

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Pick a structure

SPL expert-segmented atlas · 10 structures

Drag to rotate · scroll to zoom · click any structure. Toggle the brain shell and context nuclei to isolate what you need. Raphe and locus coeruleus are shown as bilateral markers.

3D models: SPL-PNL Brain Atlas, Surgical Planning Laboratory & Psychiatry Neuroimaging Laboratory, Brigham & Women's Hospital / Harvard (spl.harvard.edu), 3D Slicer (BSD-style) license.

Location

Cellular Neuroscience

The nerve and glial cells that matter in psychiatry — where they live, how they work normally, what goes wrong, and how a fever, a sodium of 118, or an arterial pH of 7.52 changes what they do.

Psychiatric pharmacology is usually taught as a list of receptors. That works until a patient is febrile, acidotic, hyponatraemic, or seizing — at which point you need to know which cell the receptor sits on, what that cell's metabolic reserve is, and which systemic variable it cannot tolerate. This section is organised by cell type for that reason. Eighteen populations, each with its anatomy, normal physiology, receptor and transporter complement, the diseases that are genuinely well understood, and the systemic perturbations that alter its function. Written for medical students and residents; the 3D models are procedural and rotatable. For the receptor-by-receptor companion — every transmitter, receptor family, and transporter these cells express — see the Neurotransmitter & Receptor Atlas.

Medication Comparison

Compare up to 6 medications across receptor binding, predicted side effects, and neuropsychiatric circuit targets.

⚖ Select Medications

Number to compare:

Find Similar Medications

When a medication that once worked best loses its effect (tachyphylaxis, or “poop-out”), identify the medications with the most similar pharmacology — a rational starting point for a switch. Filter by route of administration, target residual symptoms the switch must not lose ground on, and page through beyond the closest three.

Clinical decision-support only. Similarity is computed from receptor-binding profiles, action match at shared receptors (both antagonists, both reuptake inhibitors, etc.), signal-transduction tier agreement, drug class, and shared FDA indications — and, when residual symptoms are ticked, how well each candidate’s mechanism still covers them. Any axis that cannot be measured for a pair is dropped and its weight redistributed. Pharmacologic similarity does not guarantee comparable efficacy or tolerability in an individual, and for apparent tachyphylaxis a switch to a different mechanism is sometimes preferable. Use alongside clinical judgment.

FDA Indication Search

Type a diagnosis — the agents carrying an FDA-approved label for it are listed, grouped by indication and phase. Add a phase or subtype to narrow the results: Bipolar II, bipolar maintenance, acute mania, bipolar depression. Acronyms work too (MDD, OCD, GAD, PTSD).

On-label indications only. This lists FDA-approved uses recorded in the reference database; it is not a treatment guideline and does not capture the large, legitimate role of evidence-based off-label prescribing. Approval status, phase (acute vs. maintenance), line (monotherapy vs. adjunct), and approved age range are shown where known. Confirm against current prescribing information before clinical use.

Search by FDA indication

Find Complementary Medications

The mirror of “Find Similar.” For a reference medication, this surfaces two things: the curated, evidence-based combination strategies that agent participates in (TRD, treatment-resistant schizophrenia, and bipolar augmentation), and the agents that treat the same condition but act through a different receptor set — rational candidates for combination or augmentation rather than a like-for-like switch.

Clinical decision-support only. Two engines: a curated knowledge base of established combination/augmentation strategies (each tagged by evidence tier — FDA-approved adjunct, guideline, or empirical), shown above a computed ranking derived from receptor-binding divergence (30%), action divergence at shared receptors (15%), signal-transduction tier divergence (15%), drug class (15%), and shared FDA indications (25%). Contraindicated pairs (e.g. MAOI plus a serotonergic agent) are never ranked; they are listed separately with the reason. Action data (full/partial agonist, antagonist, inverse agonist, reuptake inhibitor, releaser, allosteric modulator) is curated pharmacology, not a measured constant. Neither establishes the efficacy or safety of a combination for a given patient — always assess CYP450 interactions, additive serotonergic/QT/sedation/seizure risk, and whether optimizing monotherapy is preferable. Use alongside clinical judgment.

Chem Structure

Compare two psychotropic drugs side by side — their 2D structures, molecular properties, and the fat/water, protein-binding, and receptor-binding regions that shape their behavior. Built-in lineages show how each newer-generation agent was chemically re-engineered from an older one, and why the change was expected to help.

Educational reference only. Molecular weight, formula, cLogP, polar surface area, and aqueous solubility (ESOL model) are computed with RDKit from each drug’s SMILES; structural similarity is a Morgan/ECFP4 Tanimoto score; the 3D view is a single computed conformer. Aqueous solubility is the estimated intrinsic (neutral-form) value — marketed salt forms are far more soluble. pK_a values are approximate literature figures used to estimate ionization at pH 7.4. Region annotations and “generation evolution” notes are curated teaching summaries, not a substitute for primary medicinal-chemistry sources.

Structure A

Structure B

⚡ Notable comparisons

Medication Price Comparison

Cash prices for psychiatric medications across Mark Cuban Cost Plus Drugs and HealthWarehouse, with NADAC (CMS wholesale acquisition cost) shown as a transparency anchor — most common form, 30-day supply.

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Prices reflect cash pay (no insurance) and may vary by pharmacy, dose, supply, and zip code. Generic equivalents typically used. Always verify current pricing with the source pharmacy before counseling patients. Inclusion of a pharmacy does not imply endorsement.

Medication Taper / Start Scheduler

Generate a dose titration or tapering schedule for psychiatric medications.

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Clinical Use Only — Medication tapering and titration must be supervised by a qualified prescriber. Abrupt discontinuation of psychiatric medications can cause serious withdrawal effects, relapse, or discontinuation syndrome. This tool generates reference schedules only and does not constitute medical advice. Always individualize based on patient response and clinical judgment.

💊 Single Drug Schedule

Taper (reduce dose) Start / Titrate Up

Medication

Starting Dose

Target Dose (use 0 for full taper)

Step Size

Amount to change per step

Step Interval

Time at each dose before next step

Start Date

⇋ Cross-Taper Schedule

Drug A tapers down while Drug B titrates up over the same period. Both share the same step interval and schedule dates.

↓ Drug A — Tapering Down

Medication

Starting Dose

Target Dose

Step Size

↑ Drug B — Titrating Up

Medication

Starting Dose

Target Dose

Step Size

Step Interval

For half-lives, Drug A's half-life is used

Start Date

Clinical Dementia Rating (CDR) Staging Tool

Interactive CDR calculator with box scores, global CDR derivation per Morris (1993) scoring algorithm, CDR Sum of Boxes (CDR-SB), and clinical staging interpretation.

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Clinical Use Only — The CDR should be scored based on cognitive decline from the patient's previous usual level, not impairment due to other factors such as physical handicap or depression. Score each domain independently. When ambiguous, score toward the box of greater impairment. This tool implements the standard Morris (1993) algorithm.

CDR Assessment Results

Domain	Score	Impairment Level
CDR Sum of Boxes (CDR-SB)

Summary — Copy to Clipboard

Reference: Morris JC. The Clinical Dementia Rating (CDR): current version and scoring rules. Neurology. 1993;43(11):2412-2414.
CDR-SB Staging: 0 = Normal | 0.5–4.0 = Questionable/Very Mild | 4.5–9.0 = Mild | 9.5–15.5 = Moderate | 16.0–18.0 = Severe
Note: Personal Care does not have a 0.5 score in the standard CDR. The global CDR is derived using the Washington University algorithm where Memory is the primary category. Score only as decline from previous usual level due to cognitive loss, not impairment due to other factors.

Autism Spectrum Disorder Severity Rating Tool

DSM-5 severity level assessment across both core domains (Social Communication and Restricted/Repetitive Behaviors), with clinical interpretation, support needs mapping, and screening instrument guidance.

⚠

Clinical Use Only — DSM-5 severity levels are specified independently for each core domain and reflect the current level of support required, not a fixed trait. Severity may change over time with development, intervention, and environmental context. This tool does not replace comprehensive diagnostic evaluation (ADOS-2, ADI-R, clinical interview). Co-occurring conditions (intellectual disability, ADHD, anxiety) independently affect functional presentation and must be assessed separately.

🗣 Domain A: Social Communication & Interaction

Level 1 Requiring Support

Without supports in place, deficits in social communication cause noticeable impairments. Difficulty initiating social interactions and clear examples of atypical or unsuccessful responses to social overtures of others. May appear to have decreased interest in social interactions.

Example: Speaks in full sentences, engages in communication, but to-and-fro conversation fails; attempts to make friends are odd and typically unsuccessful.

Level 2 Requiring Substantial Support

Marked deficits in verbal and nonverbal social communication skills; social impairments apparent even with supports in place; limited initiation of social interactions; and reduced or abnormal responses to social overtures from others.

Example: Speaks simple sentences, interaction limited to narrow special interests, markedly odd nonverbal communication.

Level 3 Requiring Very Substantial Support

Severe deficits in verbal and nonverbal social communication skills cause severe impairments in functioning, very limited initiation of social interactions, and minimal response to social overtures from others.

Example: Few words of intelligible speech, rarely initiates interaction, makes unusual approaches to meet needs only, responds to only very direct social approaches.

🔄 Domain B: Restricted & Repetitive Behaviors

Level 1 Requiring Support

Inflexibility of behavior causes significant interference with functioning in one or more contexts. Difficulty switching between activities. Problems of organization and planning hamper independence.

Functional impact: Executive function difficulties (task-switching, planning, organization) are often the most impairing features. Rigidity may be less visible externally but causes substantial internal distress.

Level 2 Requiring Substantial Support

Inflexibility of behavior, difficulty coping with change, or other restricted/repetitive behaviors appear frequently enough to be obvious to the casual observer and interfere with functioning in a variety of contexts. Distress and/or difficulty changing focus or action.

Functional impact: Behavioral inflexibility creates significant difficulty with transitions. Distress when expected patterns are disrupted may manifest as dysregulation across multiple settings.

Level 3 Requiring Very Substantial Support

Inflexibility of behavior, extreme difficulty coping with change, or other restricted/repetitive behaviors markedly interfere with functioning in all spheres. Great distress/difficulty changing focus or action.

Functional impact: Extreme inflexibility, intense sensory behaviors, great difficulty redirecting. Self-injurious behavior or aggression may occur with communication frustration or sensory overload.

📋 DSM-5 Diagnostic Specifiers

Check if present. These specifiers are documented alongside severity level to provide a complete diagnostic formulation.

With intellectual impairment

Specify current intellectual functioning level. ~33% of individuals with ASD have co-occurring intellectual disability (IQ <70).

With language impairment

Specify current language functioning (e.g., no intelligible speech, phrase speech only, full sentences with pragmatic deficits).

Associated with known medical/genetic condition

Document associated conditions (e.g., Fragile X, Rett syndrome, tuberous sclerosis, chromosomal abnormalities).

Associated with catatonia

Catatonia can co-occur with ASD. Specify if catatonic features are present (refer to DSM-5 catatonia criteria).

ASD Severity Assessment Results

Screening & Assessment Instruments Reference

Instrument	Type	Age Range	Administration	Key Features
M-CHAT-R/F	Screening	16–30 months	Parent questionnaire + follow-up	20 items; sensitivity 0.85, specificity 0.99 with follow-up; AAP-recommended universal screen
ADOS-2	Diagnostic	12 months – adult	Semi-structured observation (40–60 min)	Gold standard; 5 modules by age/language; calibrated severity scores (CSS 1–10); requires trained clinician
ADI-R	Diagnostic	Mental age ≥2 years	Caregiver interview (1.5–2.5 hrs)	93 items; lifetime and current behavior; strong psychometrics; used alongside ADOS-2
SRS-2	Screening/Severity	2.5 years – adult	Questionnaire (15–20 min)	65 items; T-scores: ≤59 normal, 60–65 mild, 66–75 moderate, ≥76 severe; tracks treatment response
SCQ	Screening	≥4 years (mental age ≥2)	Parent questionnaire (10 min)	40 items based on ADI-R; cutoff ≥15 suggests further evaluation; Lifetime and Current forms
CARS-2	Diagnostic/Severity	≥2 years	Clinician rating (5–10 min)	15 items; Standard (ST) and High-Functioning (HF) versions; scores: <30 non-ASD, 30–36.5 mild-moderate, ≥37 severe
ASRS	Screening	2–18 years	Parent/teacher (15 min)	70 items; DSM-5 aligned; T-score ≥60 elevated; peer-comparison and DSM-scale scores
RAADS-R	Screening (adults)	≥18 years	Self-report + clinician (30 min)	80 items; cutoff ≥65; designed for adults who may have been missed in childhood; sensitivity 0.97
CAT-Q	Camouflaging measure	≥16 years	Self-report (10 min)	25 items; measures compensation, masking, assimilation; useful for identifying underdiagnosed females

Pharmacotherapy Reference by Target Symptom

Target Symptom	First-Line	Alternatives	Notes
Irritability / Aggression	Risperidone (age ≥5), Aripiprazole (age ≥6)	N-acetylcysteine (adjunct)	Only FDA-approved medications for ASD-associated irritability; monitor metabolic parameters
Hyperactivity / Inattention	Methylphenidate (low dose)	Guanfacine ER, Atomoxetine	Lower response rate than in ADHD alone (~50% vs 75%); higher side-effect sensitivity; start low, go slow
Anxiety / Repetitive behaviors	SSRIs (fluoxetine, sertraline)	Buspirone	Limited RCT evidence in ASD; clinical experience supports use; watch for activation/agitation
Sleep disturbance	Melatonin (1–5 mg)	Trazodone, Clonidine	Melatonin has strongest evidence base in ASD; address sleep hygiene first
Self-injurious behavior	Risperidone, Aripiprazole	Naltrexone, Clonidine	Behavioral intervention is first-line; medication as adjunct for severe/refractory cases

Summary — Copy to Clipboard

Reference: American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). Arlington, VA: APA; 2013.
Note: Severity levels are rated independently for each domain and reflect current support needs, not inherent capacity. Levels may differ across the two domains and may change over time. Co-occurring intellectual disability, language impairment, and other conditions should be specified separately. The tool generates a clinical summary—it does not replace comprehensive evaluation.

Suicide Risk Assessment Tools

Clinical screening instruments for suicide ideation, behavior, and risk stratification. Three validated assessment approaches: C-SSRS Screen (rapid screening), C-SSRS Full Risk Assessment (comprehensive), and Risk/Protective Factors Framework (AFSP).

⚠ Clinical Notice: These screening tools are designed to facilitate clinical assessment and should not be used as standalone diagnostic instruments. They supplement, not replace, comprehensive clinical evaluation, risk assessment, and clinical judgment. All positive screens require immediate further evaluation by qualified mental health professionals. For crisis support: 988 Suicide & Crisis Lifeline (call or text 988, available 24/7).

References:
Posner K, Brown GK, Stanley B, et al. The Columbia-Suicide Severity Rating Scale: Initial Validity and Internal Consistency Findings from Three Multisite Studies with Adolescents and Adults. J Clin Psychiatry. 2011;72(2):233-239.
American Foundation for Suicide Prevention (AFSP). Risk factors, protective factors, and warning signs. Accessed 2026.

SLUMS Examination

Saint Louis University Mental Status Examination — 30-point cognitive screening tool for detecting mild neurocognitive disorder and dementia, with domain-specific impairment analysis.

Clinical Use Only — The SLUMS is a screening instrument and does not replace comprehensive neuropsychological evaluation. Results should be interpreted in the context of the patient's educational background, medical history, cultural factors, and baseline functioning. Sensitivity to mild cognitive impairment may exceed the MMSE (Tariq et al., 2006).

Patient Information

Education Level (affects scoring thresholds) High School Education or Higher Less Than High School Education

Q1

Orientation 1 point

"What day of the week is it?"

Correct

Q2

Orientation 1 point

"What is the year?"

Correct

Q3

Orientation 1 point

"What state are we in?"

Correct

Q4

Registration 0 points (encoding only)

"Please remember these five objects. I will ask you what they are later:"

Apple

Pen

Tie

House

Car

Encoding phase — scored in Q7 (Delayed Recall)

Q5

Executive/Attention 3 points

"You have $100 and you go to the store and buy a dozen apples for $3 and a tricycle for $20."

A. "How much did you spend?"

Correct ($23)

B. "How much do you have left?"

Correct ($77)

Q6

Language/Processing 3 points

"Please name as many animals as you can in one minute."

1:00

0–4 animals (0 pts) 5–9 animals (1 pt) 10–14 animals (2 pts) 15+ animals (3 pts)

Q7

Memory 5 points

"What were the five objects I asked you to remember? 1 point for each one correct."

Apple Pen Tie House Car

Q8

Working Memory 2 points

"I am going to give you a series of numbers and I would like you to give them to me backwards."

Practice: "87 → 78" (0 pts)

Example only

648 reversed correctly (1 pt)

648 → 846

8537 reversed correctly (1 pt)

8537 → 7358

Q9

Visuospatial/Executive 4 points

"Please put in the hour markers and set the time to 10 minutes to 11 o'clock (10:50)."

Hour markers present and correct (2 pts)

Correct

Time (10:50) set correctly (2 pts)

Correct

Q10

Attention/Perception 2 points

"Please place an X in the triangle. Which of the above figures is largest?"

X placed in triangle (1 pt)

Correct

Correctly identified largest figure (1 pt)

Correct (Square)

Q11

Memory/Executive 8 points

"I am going to tell you a story. Please listen carefully because afterwards, I'm going to ask you some questions about it."

Jill was a very successful stockbroker. She made a lot of money on the stock market. She then met Jack, a devastatingly handsome man. She married him and had three children. They lived in Chicago. She then stopped work and stayed at home to bring up her children. When they were teenagers, she went back to work. She and Jack lived happily ever after.

"What was the female's name?" (2 pts)

Correct (Jill)

"What work did she do?" (2 pts)

Correct (Stockbroker)

"When did she go back to work?" (2 pts)

Correct (When children were teenagers)

"What state did she live in?" (2 pts)

Correct (Illinois — Chicago)

0

/ 30 points

—

Cognitive Domain Analysis

Orientation / Temporal-Spatial Awareness 0/3

Brain Regions: Hippocampus, medial temporal lobe, thalamus
Clinical Significance: Orientation requires intact episodic and semantic memory circuits. Temporal disorientation often precedes spatial disorientation in Alzheimer's disease.

Executive Functioning 0/3

Brain Regions: Prefrontal cortex (dorsolateral), anterior cingulate
Clinical Significance: Scored on Q5 calculation (multi-step reasoning). Clock drawing (Q9, scored under Visuospatial) and story recall (Q11, scored under Memory) also engage executive function. Classical frontal-subcortical circuit involvement.

Attention & Concentration 0/2

Brain Regions: Frontal/parietal networks, reticular activating system
Clinical Significance: Sustained attention required for multi-step math problems; selective visual attention for shape identification. Impaired early in delirium and ADHD.

Memory — Episodic Retrieval 0/13

Brain Regions: Hippocampus, medial temporal lobe, Papez circuit
Clinical Significance: Delayed recall (Q7) and narrative memory (Q11) together comprise 13/30 points—the largest domain weight. Disproportionate memory loss relative to other domains suggests Alzheimer's-pattern impairment. Encoding failure (poor registration) vs. retrieval failure (poor recall with preserved recognition) helps distinguish cortical vs. subcortical dementia.

Working Memory 0/2

Brain Regions: Dorsolateral prefrontal cortex, posterior parietal cortex
Clinical Significance: Digit span backwards requires active manipulation of held information. Impaired in frontostriatal conditions, schizophrenia, and delirium.

Language & Verbal Skills / Processing Speed 0/3

Brain Regions: Left temporal lobe (Wernicke's area), frontal-subcortical circuits
Clinical Significance: Animal fluency is a timed semantic retrieval task that taxes both language networks and processing speed. Reduced output may reflect frontal-subcortical dysfunction (clustering/switching deficit) or temporal lobe pathology (semantic store depletion).

Visuospatial / Construction 0/4

Brain Regions: Right parietal lobe, parietal-occipital junction
Clinical Significance: Scored on Q9 clock drawing (visuospatial construction + executive planning). Shape tasks (Q10) scored under Attention. Disproportionate visuospatial impairment suggests right parietal pathology or Lewy body dementia.

Question-by-Question Results

PANSS (Positive and Negative Syndrome Scale)

Standardized clinical assessment for schizophrenia and psychosis symptom severity. Two validated approaches: PANSS-6 (brief 6-item screening) and PANSS-30 (full 30-item assessment with Positive, Negative, and General Psychopathology subscales plus Marder factor analysis).

Clinical Use Only: The PANSS requires trained rater administration. Ratings should reflect the past week. Each item is rated from 1 (Absent) to 7 (Extreme). Use in clinical context only.

Bush-Francis Catatonia Rating Scale (BFCRS)

Standardized bedside assessment for catatonia. Two approaches: 14-item Catatonia Screening Instrument (CSI) for rapid detection, and full 23-item severity rating scale (CRS) with subtype classification and malignant catatonia screening.

For clinical use only. The BFCRS is administered via standardized bedside examination. Rate items based on observed behavior. Items 12, 17–21 are scored as 0 (Absent) or 3 (Present) only.

Catatonia Screening Index (CSI)

Screen for presence of catatonia using 14 core items. Score: 2 or more items present = positive screen.

1. Immobility/Stupor

Extreme hypoactivity, immobile, minimally responsive to stimuli.

Present

2. Mutism

Verbally unresponsive or minimally responsive.

Present

3. Staring

Fixed gaze, little or no visual scanning, decreased blinking.

Present

4. Posturing/Catalepsy

Spontaneous maintenance of posture(s), including mundane.

Present

5. Grimacing

Maintenance of odd facial expressions.

Present

6. Echopraxia/Echolalia

Mimicking examiner's movements (echopraxia) or speech (echolalia).

Present

7. Stereotypy

Repetitive, non-goal-directed motor activity (e.g., finger-play, repeatedly touching, patting or rubbing self).

Present

8. Mannerisms

Odd, purposeful movements (hopping or walking tiptoe, saluting passers-by or exaggerated caricatures of mundane movements).

Present

9. Verbigeration

Stereotyped & meaningless repetition of words & phrases.

Present

10. Rigidity

Maintenance of a rigid position despite efforts to be moved (exclude if cog-wheeling or tremor present).

Present

11. Negativism

Apparently motiveless resistance to instructions or attempts to move/examine patients. Contrary behavior.

Present

12. Waxy Flexibility

During repositioning, patient offers initial resistance before allowing repositioning, similar to bending candle.

Present

13. Withdrawal

Refusal to eat, drink and/or make eye contact.

Present

14. Excitement

Extreme hyperactivity, constant motor unrest which is apparently non-purposeful. Not attributable to akathisia or goal-directed agitation.

Present

Screening Score: 0 /14

Full Rating Scale (CRS)

Complete assessment of 23 items. Severity scale 0–69. Items 12, 17–21 are binary (0 or 3).

Severity Score: 0 /69

Items Present: 0 /23

Screening Items Positive: 0 /14

CIDI 3.0 Bipolar Screening Scale

The CIDI 3.0 Bipolar Screening Scale is a brief, validated screening tool for bipolar disorder in primary care and general clinical settings. It uses stem questions about mood elevation and irritability, followed by a gate question and symptom assessment to estimate the probability of bipolar disorder. Not a diagnostic instrument—results should inform further clinical evaluation.

Clinical Note: This screening tool is designed to identify individuals at risk for bipolar disorder based on DSM-5 Criterion A and B symptoms. A positive screen does not establish diagnosis and should prompt comprehensive psychiatric evaluation including detailed history, substance use assessment, and medical workup to rule out secondary causes of mood elevation (e.g., hyperthyroidism, stimulant use, medical illness).

PCL-5 (PTSD Checklist for DSM-5)

A 20-item self-report measure assessing PTSD symptoms according to DSM-5 criteria. Items are rated 0-4 based on distress in the past month. Total scores range from 0-80, with scores ≥33 suggesting possible PTSD diagnosis.

Clinical Note: The PCL-5 is a screening tool only and does not replace clinical interview and assessment. Provisional PTSD diagnosis shown here requires confirmation through comprehensive evaluation. Use for initial assessment and treatment monitoring. A reliable change of 5 points or clinically meaningful change of 10 points indicates significant symptom shift.

YMRS (Young Mania Rating Scale)

The Young Mania Rating Scale (YMRS) is an 11-item clinician-administered scale for assessing the severity of manic symptoms in adults. Total score ranges from 0 to 60, with higher scores indicating greater manic severity. Useful for baseline assessment and monitoring treatment response in bipolar I and bipolar II disorders.

Clinical Use: This tool is for clinician assessment during interview. Ratings should reflect the patient's behavior, speech, and reported subjective experience during the assessment period. Not a substitute for full clinical evaluation.

Y-BOCS (Yale-Brown Obsessive Compulsive Scale)

Comprehensive assessment of obsessive-compulsive symptoms and severity. The Y-BOCS includes a symptom checklist to identify current and past obsessions and compulsions, plus a 10-item severity scale (items 1–10) that measures time occupied, interference, distress, resistance, and control. Supplemental items (1b, 6b) and investigational items (11–19) provide additional clinical context but are not included in the total score.

Clinical Note: The Y-BOCS is a clinician-administered scale. This tool supports structured scoring and documentation. Interpret scores in clinical context: 0–7 Subclinical, 8–15 Mild, 16–23 Moderate, 24–31 Severe, 32–40 Extreme OCD.

AIMS (Abnormal Involuntary Movement Scale)

Standardized assessment tool for detecting and monitoring tardive dyskinesia and other abnormal involuntary movements. A positive screen (score ≥2 on any item 1–7 or ≥2 on item 8) suggests need for further evaluation. Administer the complete examination procedure for accurate assessment.

Clinical Reminder: AIMS positive screen may indicate tardive dyskinesia (TD). Consider risk factors, duration of antipsychotic exposure, and patient age. TD can be irreversible; early detection and symptom management are critical. Rule out other movement disorders (e.g., Huntington's, essential tremor, Parkinson's).

Examination Procedure (Click to Expand)

Ask patient to remove anything from mouth (gum, dentures, etc.)
Ask about current condition of teeth and/or dentures
Ask if patient notices any movements in mouth, face, hands, or feet
Patient sits with hands on knees, legs slightly apart, feet flat on floor
Patient sits with hands hanging unsupported; observe for 30 seconds
Ask patient to open mouth (observe tongue at rest); repeat 2 times
Ask patient to protrude tongue (observe for abnormalities); repeat 2 times
Ask patient to tap thumb with each finger as rapidly as possible for 10–15 seconds on each hand (activated)
Examiner flexes and extends patient's left and right arms (one at a time)
Ask patient to stand (observe from all angles, including profile)
Ask patient to extend both arms out in front with palms down for 20 seconds (activated)
Have patient walk a few paces, turn, and walk back (activated)

BPRS (Brief Psychiatric Rating Scale)

18-item clinician-rated scale for psychiatric symptom severity. Each item scored 0 (not assessed) to 7 (extremely severe). Validated severity anchors: mildly ill ≈ 31, moderately ill ≈ 41, markedly ill ≈ 53 (Leucht et al., 2005).

Clinical Use Only: BPRS ratings reflect the past week based on observed behavior and verbal report. Items should be scored according to the anchor definitions provided. Not a substitute for comprehensive clinical evaluation.

ADL / IADL Functional Assessment

Evaluate activities of daily living (ADL) and instrumental activities of daily living (IADL) to assess functional independence and care needs.

Clinical Note: This checklist is for screening and documentation purposes. Score each item based on current functional status. Results should inform care planning and resource allocation.

Activities of Daily Living (ADL)

ADL Summary: 0 Independent, 0 Needs Help, 0 Dependent, 0 Cannot Do

Activity	Independent	Needs Help	Dependent	Cannot Do
Bathing	✓	✓	✓	✓
Dressing	✓	✓	✓	✓
Grooming	✓	✓	✓	✓
Mouth Care	✓	✓	✓	✓
Toileting	✓	✓	✓	✓
Transferring (Bed/Chair)	✓	✓	✓	✓
Walking	✓	✓	✓	✓
Climbing Stairs	✓	✓	✓	✓
Eating	✓	✓	✓	✓

Instrumental Activities of Daily Living (IADL)

IADL Summary: 0 Independent, 0 Needs Help, 0 Dependent, 0 Cannot Do

Activity	Independent	Needs Help	Dependent	Cannot Do
Shopping	✓	✓	✓	✓
Cooking	✓	✓	✓	✓
Managing Medications	✓	✓	✓	✓
Using Phone / Looking Up Numbers	✓	✓	✓	✓
Doing Housework	✓	✓	✓	✓
Doing Laundry	✓	✓	✓	✓
Driving / Using Public Transportation	✓	✓	✓	✓
Managing Finances*	✓	✓	✓	✓

* Financial management should never be done by the same person who is providing care.

Aid to Capacity Evaluation (ACE)

Structured 7-domain assessment of decision-specific capacity for a medical decision (Etchells et al., Joint Centre for Bioethics, University of Toronto). Yields an EMR-ready note and a printable blank form.

Capacity is decision-specific. Assess capacity for a single, specific decision. Address communication barriers (hearing, vision, language, dysphasia) and provide adequate disclosure of treatment, alternatives, risks, and consequences before scoring. People are presumed capable; if uncertain, err on the side of capable.

Assessment date:

1. Patient & Decision Context

Briefly identify the decision being assessed. Use the patient’s own words wherever possible.

Medical condition

Proposed treatment

Alternatives discussed (including refusal / withdrawal)

2. Domain Scoring

Domains 1–6: YES = appropriate response to open-ended questions; UNSURE = needs prompting with closed-ended questions; NO = cannot respond appropriately despite repeated prompting.
Domain 7 (a/b): YES means the decision is affected by depression/psychosis. Never base a finding of incapacity on domain 7 alone.

3. Overall Impression

Capacity is presumed; if uncertain, err on the side of calling the person capable.

Definitely Capable Probably Capable Probably Incapable Definitely Incapable

Comments (e.g., need for psychiatric assessment, further disclosure, family consultation)

Time taken to administer (minutes)

EMR-Ready Summary

Copied.

McLean Screening Instrument for BPD (MSI-BPD)

10-item self-report screening tool for Borderline Personality Disorder. A score of 7 or higher warrants further diagnostic evaluation.

Clinical Use: This is a screening tool, not a diagnostic instrument. A positive result should prompt comprehensive psychiatric evaluation. Use alongside clinical interview and other diagnostic criteria.

PHQ-9 (Patient Health Questionnaire-9)

Validated 9-item depression screening and severity tool. Scores range 0–27 with five severity bands. Generates an EMR-ready summary.

Clinical Use Only — The PHQ-9 is a screening and severity tool, not a standalone diagnostic instrument. Final diagnosis requires clinical interview and judgment. If Item 9 is endorsed, assess current suicidal ideation, intent, and safety.

Over the last 2 weeks, how often have you been bothered by any of the following problems?	Not at all (0)	Several days (1)	More than half the days (2)	Nearly every day (3)
1. Little interest or pleasure in doing things
2. Feeling down, depressed, or hopeless
3. Trouble falling or staying asleep, or sleeping too much
4. Feeling tired or having little energy
5. Poor appetite or overeating
6. Feeling bad about yourself — or that you are a failure or have let yourself or your family down
7. Trouble concentrating on things, such as reading the newspaper or watching television
8. Moving or speaking so slowly that other people could have noticed? Or the opposite — being so fidgety or restless that you have been moving around a lot more than usual
9. Thoughts that you would be better off dead or of hurting yourself in some way

⚠️ Item 9 endorsed — conduct a direct suicidal ideation assessment and safety evaluation before proceeding.

0

out of 27

0 / 9 answered

If you checked off any problems, how difficult have these made it for you to do your work, take care of things at home, or get along with other people?

Scoring Guide

0–4 None–Minimal None indicated 5–9 Mild Watchful waiting; repeat PHQ-9 at follow-up 10–14 Moderate Treatment plan, considering counseling, follow-up, and/or pharmacotherapy 15–19 Moderately Severe Active treatment with pharmacotherapy and/or psychotherapy 20–27 Severe Immediate pharmacotherapy; consider expedited referral to mental health specialist

GAD-7 (Generalized Anxiety Disorder 7-item Scale)

Validated 7-item anxiety screening and severity tool. Scores range 0–21 with four severity bands. Also screens for panic disorder, social anxiety, and PTSD. Generates an EMR-ready summary.

Clinical Use Only — The GAD-7 is a screening tool, not a standalone diagnostic instrument. A score ≥10 warrants further clinical evaluation. Sensitivity 89%, specificity 82% for GAD using this threshold.

Over the last 2 weeks, how often have you been bothered by the following problems?	Not at all (0)	Several days (1)	Over half the days (2)	Nearly every day (3)
1. Feeling nervous, anxious, or on edge
2. Not being able to stop or control worrying
3. Worrying too much about different things
4. Trouble relaxing
5. Being so restless that it's hard to sit still
6. Becoming easily annoyed or irritable
7. Feeling afraid as if something awful might happen

0

out of 21

0 / 7 answered

If you checked off any problems, how difficult have these made it for you to do your work, take care of things at home, or get along with other people?

Scoring Guide

0–4 Minimal Monitor; reassess as needed 5–9 Mild Watchful waiting; consider re-evaluation in 2–4 weeks 10–14 Moderate Possible anxiety disorder — consider treatment plan or referral 15–21 Severe Likely anxiety disorder — active treatment recommended

DSM-5-TR Substance Use Disorder Tool

Select a substance; the 11 DSM-5-TR criteria populate with substance-specific examples. Generates an EMR-ready text summary on completion.

Clinical Use Only — This tool is a DSM-5-TR documentation aid for licensed clinicians. Tolerance and withdrawal are excluded as criteria for hallucinogens, phencyclidine, and inhalants (max = 10). Final diagnosis requires clinical judgment and comprehensive evaluation.

Assessment date:

1. Substance

Select the specific substance being evaluated

Specify

Stimulant type

2. DSM-5-TR Criteria (past 12 months)

A problematic pattern of use leading to clinically significant impairment or distress, as manifested by 2 or more of the following within a 12-month period.

Criteria met: 0 / 11

3. Remission & Additional Specifiers

Remission status (only if full criteria previously met but no longer met) In early/recent remission (≥3 but <12 months; craving may still be present) In sustained remission (≥12 months; craving may still be present)

Additional specifiers In a controlled environment On maintenance therapy

4. Supporting notes (optional, appended to output)

EMR-Ready Summary

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Medication History Form

Comprehensive psychiatric medication history — documents prior trials, experiences, side effects, and generates a structured EMR-ready summary with failed-trial overlap analysis.

Clinical Use: This form is intended to capture a patient's prior medication experience. Leave any medication untouched if not tried. Only medications marked "Tried" will appear in the generated report.

Loading medication list…

CIWA-Ar (Alcohol Withdrawal Assessment)

The Clinical Institute Withdrawal Assessment for Alcohol, Revised (CIWA-Ar) is a 10-item, clinician-rated tool for assessing severity of acute alcohol withdrawal. Total score ranges from 0 to 67. Higher scores indicate more severe withdrawal and greater risk for seizures and delirium tremens. Commonly used to guide symptom-triggered benzodiazepine dosing protocols.

Clinical Use: CIWA-Ar is validated for adults with known alcohol withdrawal; it assumes the patient can communicate and is not heavily sedated. Patients with impaired consciousness, acute medical illness, or severe comorbidity (e.g., hepatic encephalopathy, head trauma) may require fixed-dose regimens instead of symptom-triggered protocols. Score ≥15 signals impending delirium tremens and warrants urgent treatment.

COWS (Clinical Opiate Withdrawal Scale)

The Clinical Opiate Withdrawal Scale (COWS) is an 11-item clinician-administered instrument that reproducibly rates common signs and symptoms of opiate withdrawal. It is used to quantify withdrawal severity, monitor trajectory, and guide the timing of buprenorphine induction. Total score ranges approximately 0–48; severity bands: 5–12 mild, 13–24 moderate, 25–36 moderately severe, >36 severe.

Clinical Use: Rate each item based on its apparent relationship to opiate withdrawal (e.g., do not count a fast pulse from recent exertion). A COWS score of approximately ≥8 with short-acting opioids, or ≥12–13 with long-acting opioids such as methadone, is traditionally used as the threshold for starting buprenorphine to minimize precipitated withdrawal. Always couple with clinical judgment, last-use history, and local protocol.

Adult ADHD Self-Report Scale (ASRS v1.1)

18-item screening tool for adult ADHD. Part A (6 items) is the primary screener; Part B (12 items) provides supplemental diagnostic information.

Clinical Use: A positive Part A screen (4+ items in the shaded range) warrants comprehensive ADHD evaluation. Part B frequency counts provide additional clinical cues. Not a substitute for professional diagnosis.

Epworth Sleepiness Scale (ESS)

Assess daytime sleepiness across 8 common situations. A simple screening tool to identify excessive daytime somnolence.

Clinical Note: This tool screens for daytime sleepiness and is not diagnostic. Elevated scores warrant formal sleep evaluation and physician consultation.

Instructions: Rate each situation for your likelihood of dozing off or falling asleep, not just feeling tired. Even if you haven't done some recently, estimate how they would affect you.

Situation	Would never nod off (0)	Slight chance (1)	Moderate chance (2)	High chance (3)
1. Sitting and reading
2. Watching TV
3. Sitting, inactive, in a public place (e.g., meeting, theater, dinner event)
4. As a passenger in a car for an hour or more without a break
5. Lying down to rest when circumstances permit
6. Sitting and talking to someone
7. Sitting quietly after a meal without alcohol
8. In a car, while stopped for a few minutes in traffic or at a light

0

/ 24

Answer all items to see interpretation

Burnout Assessment Tool (BAT)

The Burnout Assessment Tool (BAT) is a validated 23-item (work-related) or 22-item (general) self-report measure of burnout across four core dimensions: exhaustion, mental distance, cognitive impairment, and emotional impairment. An additional 10-item secondary symptoms scale covers psychological and psychosomatic complaints. Developed by Schaufeli, De Witte & Desart (2019) at KU Leuven. Scored 1–5 (Never to Always); domain mean scores are reported.

Clinical Use: The BAT is a screening instrument, not a diagnostic tool. Elevated scores warrant further clinical evaluation. This tool is for healthcare professionals and should be interpreted within the context of a comprehensive clinical assessment. Reference: Schaufeli, W.B., De Witte, H. & Desart, S. (2019). BAT – Test Manual. KU Leuven.

0.00

/ 5.00

No/very low risk

0.00

Exhaustion

0.00

Mental Distance

0.00

Cognitive Impairment

0.00

Emotional Impairment

0.00

Secondary Symptoms

Interpretation Guide (Mean Scores)

1.00 – 1.49 No/very low risk of burnout 1.50 – 2.49 Low risk — some burnout symptoms present 2.50 – 3.49 At risk — clinically meaningful burnout symptoms 3.50 – 4.49 High risk — significant burnout warranting intervention 4.50 – 5.00 Very high risk — severe burnout, urgent clinical attention

SMI-FRAIL-20: Medical Frailty Documentation Tool

A 20-item structured checklist to support individualized documentation of medical frailty in patients with severe mental illness (SMI), developed in response to the June 2026 CMS interim final rule (CMS-2454-IFC) narrowing the Medicaid work-requirement medical frailty exemption. Includes an optional 8-item substance use disorder (SUD) add-on module. Generates an EMR-ready summary.

Clinical & Documentation Use Only — SMI-FRAIL-20 is an educational documentation aid, not a validated psychometric instrument and not endorsed by CMS or any state Medicaid agency. It does not determine exemption eligibility; verification standards are set independently by each state. CMS's rule prohibits relying on diagnosis codes alone — pair every item scored 2–3 with a concrete, dated behavioral example in the chart note.

Policy context: CMS's June 2026 interim final rule requires states to verify not just a qualifying diagnosis but that the condition significantly impairs the patient's ability to meet the 80-hour/month Medicaid community engagement requirement. Complete this tool based on functioning over the preceding 30–90 days, using chart review, collateral information, and direct interview.

Primary psychiatric diagnosis (DSM-5-TR)

0

/ 60

Minimal impairment

0 / 15

Symptom Acuity & Safety

0 / 15

Functional Capacity

0 / 15

Care Utilization & Treatment

0 / 15

Support & Systemic Factors

Clinician-documented example of functional impairment (required for individualized documentation)

Describe one specific, dated, behavioral example — not a restated diagnosis. Cite your source (chart review, collateral, direct observation). Example: "Per residential staff report on 6/2/26, patient required prompting for hygiene on 4 of 7 days and missed a scheduled volunteer shift during a symptom exacerbation."

Patient has an active or clinically significant recent substance use disorder — include SUD Add-On Module

Under the CMS rule, the SUD frailty category applies whether or not the patient is currently in active treatment, but excludes individuals in stable, sustained recovery for five or more years.

SMI Frailty Score Interpretation (0–60)

0–10 Minimal Exemption unlikely to be supported on this domain alone; continue routine monitoring. 11–25 Mild-to-moderate May support a determination if impairment is concentrated in items 3, 4, 9, 18, 20. Narrative detail is essential. 26–40 Moderate-to-severe Generally supports a medical frailty determination. Document ADL/IADL, safety, and hospitalization findings. 41–60 Severe Strongly supports a medical frailty exemption. Document safety risk and inability to sustain 80 hrs/month of activity.

SUD Add-On Module Interpretation (0–24)

0–6 Low Low frailty contribution from SUD alone; combine with the SMI Frailty Score above. 7–14 Moderate Supports frailty determination when combined with SMI domains. 15–24 Severe Substance-related impairment may independently support a frailty determination.

These bands are a clinical organizing framework, not a CMS-published cutoff. States retain discretion over verification criteria — always pair the total score with item-level narrative. Sources: CMS, "Medicaid Community Engagement Requirement for Certain Individuals," Interim Final Rule CMS-2454-IFC (June 1, 2026); KFF, "The Medical Frailty Exemption from Medicaid Work Requirements" (June 23, 2026); Georgetown University Center for Children and Families (July 9, 2026). A multistate legal challenge to the rule is pending — confirm current enforcement status with your state Medicaid agency.

Autism Screening (AQ)

The Autism Spectrum Quotient (AQ) is a self-report screening instrument developed by Baron-Cohen et al. (2001) at the Autism Research Centre, University of Cambridge. The AQ-10 is a brief 10-item screener for rapid identification of adults who may benefit from a full autism evaluation. The AQ-50 provides a comprehensive 50-item assessment across five domains: social skills, attention switching, attention to detail, communication, and imagination. Items are scored 0 or 1 based on endorsement direction; higher scores indicate greater autistic traits.

Clinical Use: The AQ is a screening instrument, not a diagnostic tool. Elevated scores warrant formal diagnostic evaluation using DSM-5 criteria and clinical interview. This tool is for healthcare professionals and should be interpreted within the context of a comprehensive clinical assessment.
Reference: Baron-Cohen, S., Wheelwright, S., Skinner, R., Martin, J., & Clubley, E. (2001). The Autism-Spectrum Quotient (AQ): Evidence from Asperger syndrome/high-functioning autism, males and females, scientists and mathematicians. Journal of Autism and Developmental Disorders, 31(1), 5–17.

0 of 10 items answered

0

/ 10

Low

Interpretation Guide

AQ-10 (Short Screener) 0 – 5 Low — few autistic traits endorsed 6 – 10 Elevated — consider referral for comprehensive autism evaluation AQ-50 (Full Assessment) 0 – 25 Low — non-significant autistic traits 26 – 31 Borderline/Elevated — above average autistic traits, consider further evaluation 32 – 50 Clinically significant — strong indication, formal evaluation recommended

Therapy Courses

A practical, step-by-step course for clinicians, trainees, and advanced students — how to actually deliver the core techniques of the behavioral therapies with fidelity, adapt them, and measure progress.

Educational use — This course supports supervised skill development. It does not replace formal training, certification, or clinical supervision, and the interactive worksheets are teaching aids, not validated instruments.

What this course does

Most therapy training explains what a treatment is. This course focuses on how to run it: structuring sessions, assigning and reviewing homework, troubleshooting the moments where technique breaks down, and tracking outcomes. Each module pairs a concise didactic “how-to” with interactive worksheets and goal-setting tools you can use in session or in role-play.

Course learning objectives

By the end, participants will be able to: conduct functional assessments and build individualized formulations; deliver key techniques of each therapy with high fidelity; structure sessions and manage homework; adapt protocols for age, development, comorbidity, culture, and setting; select and use outcome measures; and recognize when to refer or combine approaches (including with medication).

Modules

MODULE 1 · AVAILABLE NOW

Foundational Principles of Behavioral & Cognitive-Behavioral Therapy

ABC model, reinforcement, the cognitive model, functional analysis, case formulation, session structure, measurement, and a Socratic toolkit — the shared core for every module.

MODULE 2 · AVAILABLE NOW

ABA & Related Approaches for Autism Spectrum Disorder

Discrete Trial Training with a live trial-data grid, Pivotal Response Training & ESDM planning, functional behavior assessment & FCT, and progress tracking — delivered assent-based and neurodiversity-affirming.

MODULE 3 · AVAILABLE NOW

Behavioral Activation & CBT for Depression

Full how-to: the depression cycle, activity & mood monitoring, values, graded activity scheduling, TRAP→TRAC, goal setting, and fidelity/outcome tracking — with interactive worksheets.

MODULE 4 · AVAILABLE NOW

Exposure-Based CBT for Anxiety Disorders (incl. ERP for OCD)

Inhibitory-learning model, functional assessment, SUDS hierarchy, expectancy-tracking exposure log, ERP mapping for OCD, and outcome tracking — with interactive worksheets.

MODULE 5 · AVAILABLE NOW

CBT for Anger Management & Parent Management Training

Anger log, cognitive restructuring, arousal reduction & stress inoculation; the coercive cycle, positive attending, effective commands, and consequence systems — with interactive worksheets.

MODULE 6 · AVAILABLE NOW

CBT for Psychosis (CBTp) & Related Approaches

Engagement & normalizing, ABC + 4 Ps formulation, working with voices (beliefs-about-voices) and delusions (evidence & behavioral experiments), functioning goals, and a staying-well plan — with interactive worksheets.

MODULE 7 · AVAILABLE NOW

Integration, Advanced Topics & Implementation

Transdiagnostic formulation & sequencing, combining therapy with medication, fidelity & supervision, telehealth & stepped care, and a capstone action plan — with interactive planners.

MODULE 8 · AVAILABLE NOW

EMDR Therapy for Trauma & PTSD

The eight-phase protocol as a how-to: three-pronged target sequencing & floatback, Phase 2 stabilization (calm place, container, RDI), NC/PC + SUDS/VOC assessment, and a set-by-set reprocessing log — evidence-forward, with interactive worksheets.

Format: 8–12 modules blending didactic instruction, interactive worksheets, goal setting, role-play, and case formulation. Recommended contact hours: 20–40 depending on depth. Final assessment: a written case formulation plus a live or recorded demonstration of two techniques from different modules. Every module also includes blank printable worksheets (PDF) you can hand out — look for the download link at the top of each module.

Module 3 — Behavioral Activation & CBT for Depression

A practical how-to for delivering Behavioral Activation, with interactive worksheets and goal-setting tools. ← Back to course overview · ↓ Download blank worksheets (PDF)

Educational use — Teaching module for supervised skill development. Interactive worksheets are practice aids, not validated instruments, and do not replace clinical judgment or supervision.

Module 4 — Exposure-Based CBT for Anxiety Disorders (incl. ERP for OCD)

A practical how-to for delivering exposure therapy with the inhibitory-learning model, with interactive worksheets and goal-setting tools. ← Back to course overview · ↓ Download blank worksheets (PDF)

Educational use — Teaching module for supervised skill development. Interactive worksheets are practice aids, not validated instruments, and do not replace clinical judgment or supervision. Exposure and ERP should be learned under supervision.

Module 2 — ABA & Naturalistic Approaches for Autism Spectrum Disorder

A practical, assent-based, neurodiversity-affirming how-to for Discrete Trial Training, PRT/ESDM, and function-based support, with interactive worksheets. ← Back to course overview · ↓ Download blank worksheets (PDF)

Educational use — Teaching module for supervised skill development. Interactive worksheets are practice aids, not validated instruments. ABA-based intervention should be planned and supervised by a qualified behavior analyst, with the learner’s assent and wellbeing central.

Module 6 — CBT for Psychosis (CBTp) & Related Approaches for Schizophrenia

A practical, collaborative, normalizing how-to for CBTp — formulation, working with voices and beliefs, functioning goals, and staying-well planning, with interactive worksheets. ← Back to course overview · ↓ Download blank worksheets (PDF)

Educational use — Teaching module for supervised skill development. Interactive worksheets are practice aids, not validated instruments. Where psychotic symptoms involve risk (e.g., command hallucinations, persecutory beliefs driving action), prioritize risk assessment, safety planning, and coordination with the treating team.

Module 1 — Foundational Principles of Behavioral & Cognitive-Behavioral Therapy

The shared core: behavioral & cognitive principles, functional analysis, case formulation, session structure, measurement, and Socratic method. ← Back to course overview · ↓ Download blank worksheets (PDF)

Educational use — Teaching module for supervised skill development. Interactive worksheets are practice aids, not validated instruments.

Module 5 — CBT for Anger Management & Parent Management Training

Two routes to reducing anger, irritability, and aggression: CBT for anger (adults/adolescents) and PMT for caregivers, with interactive worksheets. ← Back to course overview · ↓ Download blank worksheets (PDF)

Educational use — Teaching module for supervised skill development. Screen for safety (domestic violence, abuse) before recommending techniques; where aggression poses risk, prioritize safety planning and referral.

Module 7 — Integration, Advanced Topics & Implementation

Sequencing therapies, combining with medication, fidelity & supervision, telehealth & stepped care, and a capstone action plan. ← Back to course overview · ↓ Download blank worksheets (PDF)

Educational use — Teaching module for supervised skill development. Interactive worksheets are planning aids; prescribing and clinical decisions rest with the treating clinician.

Module 8 — EMDR Therapy for Trauma & PTSD

Alcohol Use Disorder

Standard drinks and limits, the dangers of withdrawal, medications, and skills to cut back.

Open handout →

Opioids

Opioid Use Disorder

Overdose and naloxone, life-saving medications, withdrawal, and harm reduction.

Open handout →

Cannabis

Cannabis Use

When use becomes a problem, effects of regular use, withdrawal, and cutting back.

Open handout →

Nicotine

Nicotine Dependence

Why quitting is hard, medications that double your odds, quit-day planning, and cravings.

Open handout →

Stimulants

Methamphetamine Use Disorder

What meth does, health effects, what treatment works, and the crash and early recovery.

The tyramine diet, dangerous drug interactions, washout periods, and blood pressure.

Open handout →

Medications · Antipsychotics

Antipsychotic

Atypical (2nd-Gen) Antipsychotics

Metabolic and movement effects, the dementia warning, and the full monitoring schedule.

Open handout →

Antipsychotic

Why the dose goes up slowly, the serious-rash warning, and interactions.

Open handout →

Anticonvulsant

Valproate (Depakote)

Liver, pancreas, and pregnancy warnings, plus LFT, platelet, and level monitoring.

Open handout →

Anticonvulsant

Carbamazepine (Tegretol)

Rash and blood-count warnings, HLA-B*1502 testing, drug interactions, and monitoring.

Open handout →

Anticonvulsant

Oxcarbazepine (Trileptal)

The low-sodium and serious-rash cautions, interactions, and sodium monitoring.

Open handout →

Anticonvulsant

Gabapentin & Pregabalin

Breathing risk with opioids, dependence, kidney dosing, and common side effects.

Open handout →

Medications · Sedatives & Stimulants

Sedative

Benzodiazepines

The opioid and dependence warnings, alcohol danger, and why never to stop abruptly.

Open handout →

Stimulant

Stimulants (ADHD)

Timing to protect sleep, the misuse warning, and heart, blood-pressure, and growth checks.

Open handout →

Sleep

Sleep Medications (Z-Drugs)

Taking them safely, the complex-sleep-behavior warning, and dependence.

Open handout →

Medications · Antihistamines & Anticholinergics

Antihistamine / Anticholinergic

Antihistamines & Anticholinergics

Benadryl, Vistaril, and Cogentin: uses, anticholinergic side effects, and cautions in older adults.

Open handout →

Printable Clinical Forms

Download and print blank rating scales for bedside or clinic use.

Documentation Tools

Psychiatric History & MSE (1-page)

PsychoPharmRef one-page intake worksheet

Four-quadrant H&P: CC/HPI/ROS, background (psychosocial, SUD, allergies, PMH/PSH, FH, PPH), MSE/vitals/labs, and diagnosis/assessment/plan.

Psychiatric SOAP Follow-up (1-page)

PsychoPharmRef one-page progress-note worksheet

Subjective (mood/anxiety/sleep/SI/HI/adherence/side effects), Objective (vitals + key MSE + scales), Assessment (course + risk), Plan (meds, therapy, labs, follow-up).

Medication Safety & Monitoring

Tisdale QT Risk Score

Tisdale JE, et al. Circ Cardiovasc Qual Outcomes. 2013;6(4):479-487

Checklist for QT-prolonging drug risk stratification in acute care settings.

Cognitive & Neurodevelopmental

Clinical Dementia Rating (CDR)

Morris JC. Neurology. 1993;43(11):2412-2414

Clinician-administered staging scale for dementia severity across 6 cognitive domains.

Autism Quotient (AQ-10)

Baron-Cohen S, et al. J Autism Dev Disord. 2001;31(1):5-17

10-item screening for autism spectrum traits. Cutoff ≥6 suggests referral for evaluation.

ASRS v1.1 (Adult ADHD)

Kessler RC, et al. Psychol Med. 2005;35(2):245-256

18-item self-report ADHD screening with Part A (6 items) and Part B (12 supplemental).

Aid to Capacity Evaluation (ACE)

Etchells E, et al. Joint Centre for Bioethics, U. of Toronto. (CMAJ 1996;155:657-61)

Structured 7-domain assessment of decision-specific capacity for a medical decision (understanding, appreciation, and affective influences).

Mood & Anxiety

CIDI 3.0 Bipolar Screening

Kessler RC, et al. Am J Psychiatry. 2006;163(10):1762-1769

Structured bipolar disorder screening with stem questions and 9 Criterion B symptoms.

Young Mania Rating Scale (YMRS)

Young RC, et al. Br J Psychiatry. 1978;133:429-435

Clinician-rated 11-item scale for assessing manic symptom severity (0-60).

PCL-5 (PTSD Checklist)

Weathers FW, et al. National Center for PTSD. 2013

20-item PTSD symptom checklist across 4 DSM-5 clusters. Cutoff ≥33 suggests PTSD.

Y-BOCS (OCD Severity)

Goodman WK, et al. Arch Gen Psychiatry. 1989;46(11):1006-1011

Clinician-rated 10-item scale for obsessive-compulsive symptom severity (0-40).

MSI-BPD (Borderline Screening)

Zanarini MC, et al. J Clin Psychiatry. 2003;64(5):566-569

10-item self-report screening for borderline personality disorder. Cutoff ≥7 positive.

Psychosis & Movement Disorders

PANSS-6 (Brief Psychosis)

Kay SR, et al. Schizophr Bull. 1987;13(2):261-276

6-item abbreviated PANSS with positive, negative, and composite subscales (0-42).

PANSS-30 (Full Psychosis)

Kay SR, et al. Schizophr Bull. 1987;13(2):261-276

Comprehensive 30-item scale with positive, negative, and general psychopathology subscales.

BFCRS (Catatonia Rating)

Bush G, et al. Acta Psychiatr Scand. 1996;93(2):129-137

CSI (14 items) + CRS (23 items) for catatonia screening and severity assessment.

AIMS (Dyskinesia Rating)

Guy W. ECDEU Assessment Manual. 1976

10-item scale assessing abnormal involuntary movements from antipsychotic exposure (0-28).

Sleep & Alertness

Epworth Sleepiness Scale (ESS)

Johns MW. Sleep. 1991;14(6):540-545

8-item self-report of daytime sleepiness across common situations (0-24).

Safety & Risk Assessment

Suicide Risk Assessment

Posner K, et al. J Clin Psychiatry. 2011;72(2):233-239

C-SSRS screening + risk/protective factors for comprehensive suicide risk assessment.

C-SSRS Full Version

Posner K, et al. Am J Psychiatry. 2011;168(12):1266-1277

Complete Columbia-Suicide Severity Rating Scale — 5 sections: risk/protective factors, ideation (5 levels), intensity, behavior, and lethality.

Wellness & Burnout

BAT — Work Version

Schaufeli WB, et al. Assessment. 2020;27(7):1506-1521

23-item Burnout Assessment Tool measuring work-related burnout across 6 domains (1-5 scale).

BAT — General Version

Schaufeli WB, et al. Assessment. 2020;27(7):1506-1521

22-item Burnout Assessment Tool for general (non-work) burnout across 6 domains (1-5 scale).

Chapters

103 evidence-based clinical articles on psychopharmacology, psychiatric disorders, clinical practice, and more.

Browse all articles with search, filtering, and category organization on the full blog page.

Browse All 103 Articles →

Psychopharmacology

Antidepressants, antipsychotics, mood stabilizers, benzodiazepines, clozapine, pharmacogenomics

Mood & Anxiety

MDD, bipolar, panic/GAD, PTSD, OCD, social anxiety, adjustment disorder

Addiction & SUDs

Alcohol, opioids, cannabis, stimulants, smoking cessation, motivational interviewing

Clinical Practice

Psychiatric interview, ethics, emergency psych, forensic, capacity, telepsychiatry

Neuroscience & Neuro

Neuroscience foundations, delirium, catatonia, TBI, Alzheimer’s, Parkinson’s, FTD

Special Topics

ECT, ketamine, pregnancy, geriatrics, eating disorders, dissociative, sleep, nutrition

Medical Education & Foundations

Learning science, behavioral modification, pharmacokinetics, statistics, journal articles, medication discovery

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Columbia-Suicide Severity Rating Scale: Screen Version

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