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.

101
Total Medications
26
Antidepressants
26
Antipsychotics
7
Mood Stabilizers
9
Sleep Medications
30
QT Prolonging
Start with your task

Seven core clinical tasks. Open one to follow its pathway to the right tool, scale, or chapter.

1 Diagnostic assessment Screen, confirm, and characterize a psychiatric diagnosis.
2 Risk assessment Identify acute safety, medical, and treatment-emergent risk.
3 Follow-up assessment Track response and monitor safety over time.
1
Re-measure symptom trajectory
3
Adherence & function
4 Choosing appropriate therapies Select an evidence-based first-line treatment.
5 Refining therapeutic choices Optimize when the first choice falls short.
1
Reassess response & tolerability
3
Pharmacology-guided fine-tuning
6 Managing therapeutic risks Anticipate and mitigate side effects and known hazards.
1
Screen interactions
3
Recognize serious reactions
4
Educate the patient
7 Personalizing care Tailor treatment to the individual patient.

Drug Database

Drug 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

Diagnoses Database

Sortable, filterable reference of psychiatric diagnoses. Click any row for key characteristics, DSM-5-TR / ICD-10-CM / ICD-11 codes, approved & adjunct medications, recommended therapy, epidemiology, differentials, red flags, and rating scales.

Reference for clinical judgment. Medications are FDA-approved for the listed diagnosis unless marked off-label. Epidemiologic figures are approximate; codes follow ICD-10-CM FY2026 and ICD-11. Last clinically reviewed October 2, 2026. Not a substitute for clinical assessment.
Diagnosis Category ICD-10-CM / DSM-5-TR ICD-11 Prevalence Age of Onset First-line Treatment

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
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 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.

vs

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.

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.

Curves use a simplified Bateman equation (single-compartment oral absorption model). Peak height is proportional to primary receptor binding affinity. Actual pharmacokinetics vary with food, genetics, formulation, drug interactions, and individual metabolism. Not for clinical dosing decisions.

Medication Price Comparison

Cash prices for common strengths from Mark Cuban Cost Plus Drugs and HealthWarehouse, with the CMS NADAC wholesale cost shown as a reference point. Each row lists the strength and quantity priced (based on usual dosing, roughly a 30-day supply).

Prices as of: —
Loading pricing data…

Brand-name drugs: check the manufacturer’s savings program; retail cash prices are shown when a pharmacy stocks the product.

Prices are cash pay (no insurance) for the listed strength and quantity, and change often; they may vary by pharmacy and zip code. NADAC is what pharmacies pay wholesale, not a price a patient can buy at, so it is excluded from “Best.” Because NADAC is an average of what many pharmacies pay, a low-markup seller like Cost Plus Drugs can come in below it for some generics. Cost Plus prices include its markup and $5 pharmacy fee but not shipping. Cost Plus Drugs does not sell controlled substances. Insurance copays or discount coupons may be lower. Always verify current pricing with the pharmacy before counseling patients. Inclusion of a pharmacy does not imply endorsement. Not medical or financial advice.

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.

▶ Tisdale QT Risk Score

Validated risk scoring tool for predicting QT prolongation in hospitalized patients (Tisdale et al., Circ Cardiovasc Qual Outcomes, 2013). Each item adds to a cumulative risk score.

Originally validated in inpatient settings. Use in outpatient context as a general guide to identify high-burden patients.

Total Score: 0 —

▶ 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

  1. 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.
  2. 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.
  3. Academy of Consultation-Liaison Psychiatry (ACLP). How-To Guide: QTc Prolongation. 2020. Available at: aclponline.org.
  4. Woosley RL, Heise CW, Gallo T, et al. CredibleMeds / AZCERT. Available at: crediblemeds.org. [QTDrugs List — updated continuously]
  5. Nachimuthu S, Assar MD, Schussler JM. Drug-induced QT interval prolongation: mechanisms and clinical management. Ther Adv Drug Saf. 2012;3(5):241–253.
  6. Roden DM. Drug-Induced Prolongation of the QT Interval. N Engl J Med. 2004;350:1013–1022.
  7. 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.

⚙ Usage Calculator

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

▶ Forward Refill Dates

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

◀ Reverse Refill Tracker

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

🔄 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
Medication B
Leave blank to auto-align to the latest depletion date

Cognitive Domains

Cognitive domains, standardized screening instruments, and clinical interpretation.

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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 →DLPFCOFC/vmPFCACCStriatumMD thalamusNAccVTA/SNcOpen 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 · Haber, 2016
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 →DLPFCACCAmygdalaHippocampusStriatumMD thalamusNAccVTA/SNcOpen 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
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
■ 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
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
■ 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
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
■ 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.
■ Neurodevelopmental Disorders Fronto-striatal attention • Social brain network • Connectivity differences
ADHD
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.
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).
■ 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)
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)
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)
■ 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)
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
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

📈 Network → Disorder Quick Reference

Network / CircuitPrimary DisordersKey Brain Regions
Amygdala Fear NetworkPTSD, GAD, Panic DisorderAmygdala, vmPFC, hippocampus, BNST
Orbitofrontal LoopOCD, Tourette, FTD (behavioral)OFC, caudate, thalamus, ACC
Frontostriatal Attention NetworkADHD, Schizophrenia (cognitive), MDDDLPFC, caudate/putamen, ACC, cerebellum
Subgenual / Mood NetworkMDD, Bipolar DisordersgACC, vmPFC, amygdala, NAc
Reward Network (Striatum)Bipolar (mania), Addiction, MDD (anhedonia)NAc, VTA, OFC, ventral striatum
DLPFC Cognitive NetworkSchizophrenia (negative/cognitive), ADHDDLPFC, thalamus, dorsal striatum
Memory Network (Hippocampus)Alzheimer, Korsakoff, PTSDHippocampus, entorhinal cx, mammillary bodies, thalamus
Social Brain NetworkASD, Social Anxiety DisorderSTS, fusiform, amygdala, mPFC
Nigrostriatal Motor NetworkParkinson, Huntington, Tardive DyskinesiaSNpc, putamen, GPi, motor cortex

📚 References

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

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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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.

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Medication Comparison

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

⚖ Select Medications

Number to compare:

Tolerability Comparison

Compare the relative side-effect profiles of two to four medications side by side, then switch between a clinician view (full tiers, incidence, class safety) and a simplified patient handout view for chairside discussion.

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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 show more matches six at a time.

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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).

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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.

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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.

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Medication Taper / Start Scheduler

Generate a dose titration or tapering schedule for psychiatric medications.

⚠
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

Amount to change per step
Time at each dose before next step

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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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.

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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).

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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.

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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).

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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.

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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.

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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.

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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.

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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.

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AIMS (Abnormal Involuntary Movement Scale)

Standardized assessment tool for detecting and monitoring tardive dyskinesia and other abnormal involuntary movements. A positive screen (Schooler–Kane: ≥2 on two or more of items 1–7, or ≥3 on any one) suggests need for further evaluation. Administer the complete examination procedure for accurate assessment.

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Movement Disorder Assessment

A structured bedside phenomenology exam: describe every movement on the seven descriptive axes, match a signature to a category, and copy a description-first chart note. Built on The Movement Disorder Examination: A Region-by-Region Phenomenology Atlas. A documentation aid, not a diagnostic device.

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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).

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ADL / IADL Functional Assessment

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

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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.

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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.

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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.

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

Validated 7-item anxiety screening and severity tool. Scores range 0–21 with four severity bands. At ≥10 it also detects panic disorder, social anxiety, and PTSD with moderate sensitivity (about 66–74%; Kroenke 2007). Generates an EMR-ready summary.

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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.

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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.

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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.

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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.

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24-Hour Caffeine Intake Calculator

Document the caffeine-containing products a patient used over a 24-hour period to estimate total caffeine intake in milligrams. Per-serving values are typical estimates and can be edited to match a specific brand or brew strength.

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24-Hour THC Intake Calculator

Document the cannabis products a patient used over a 24-hour period to estimate total THC content in milligrams. Flower, vape oil and concentrate are entered as amount × potency; edibles, beverages and tinctures are entered as milligrams per unit × units.

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24-Hour Alcohol Intake Calculator

Document the alcoholic beverages a patient used over a 24-hour period to total US standard drinks and grams of ethanol. Preset volumes and ABV are editable to match the actual drink.

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Anticholinergic Burden Assessment

Build a patient’s medication list from a searchable library of anticholinergic agents to see the cumulative burden on two validated scales — the Anticholinergic Cognitive Burden (ACB) scale and the Anticholinergic Risk Scale (ARS) — with older-adult (≥65) flags and an EMR-ready report.

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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.

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Epworth Sleepiness Scale (ESS)

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

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Insomnia Severity Index (ISI)

Seven-item self-report measure of insomnia severity over the past two weeks (Morin). Total 0–28 across four severity bands. First-line treatment for chronic insomnia is CBT-I.

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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.

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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.

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DV / IPV Assessment

A point-of-care intimate partner violence tool combining the validated HITS screen (Hurt, Insult, Threaten, Scream) with a structured, evidence-based lethality / danger review. Generates an EMR-ready summary. Use it to support recognition, danger assessment, and safety planning — see the Domestic & Intimate Partner Violence chapter for clinical context.

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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.

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OTC & Non-Prescription Sleep Aid Comparison

Compare non-prescription sleep aids side by side — OTC antihistamines, melatonin, herbals, minerals and amino acids, and cannabis — by mechanism, typical dose, onset/duration, evidence grade, key risks, and interactions. Filter by category or evidence and flag agents to avoid in older adults.

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Fatigue / Low Energy Workup

A tiered symptom and red-flag checklist that builds a suggested laboratory workup and differential for low energy, with an urgent-evaluation flag for red flags and an EMR-ready summary. Covers non-psychiatric causes across every organ system.

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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.

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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)  ·  Measure baseline severity with the ISI →

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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)

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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)

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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)

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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)

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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)

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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)

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Module 8 — EMDR Therapy for Trauma & PTSD

A practical how-to for the eight-phase EMDR protocol — target sequencing, stabilization & resourcing, NC/PC and SUDS/VOC assessment, and set-by-set reprocessing, with interactive worksheets. ← Back to course overview  ·  ↓ Download blank worksheets (PDF)

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Module 9 — CBT for Insomnia (CBT-I)

A practical how-to for delivering first-line CBT for chronic insomnia — the 3-P formulation, sleep restriction with weekly titration, stimulus control, and cognitive restructuring, with interactive worksheets and a live sleep-efficiency calculator. ← Back to course overview  ·  ↓ Download blank worksheets (PDF)

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Module 10 — Marriage & Couples Therapy

A practical how-to for treating marriage and other committed couples: safety and assessment, the major evidence-based models, couple-based protocols for individual disorders, and the ethics of secrets and documentation, with interactive worksheets. ← Back to course overview  ·  ↓ Download blank worksheets (PDF)

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Question Bank

1,494 USMLE-style psychiatry questions across 32 categories and 120 source chapters. Sign in to start a quiz.

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Handouts

Plain-language, one-page handouts you can view here or download as a PDF to give patients. Each opens in its own page with a Download / Print PDF button.

Therapy
Sleep

Understanding Insomnia & Sleep Hygiene

What insomnia is and the behavioral habits that retrain the brain for sleep.

Open handout →
Anxiety

Calming Your Fight-or-Flight Response

The biology of anxiety plus fast skills: square breathing and 5-4-3-2-1 grounding.

Open handout →
Crisis Planning

My Safety Plan

A fill-in safety plan: warning signs, coping steps, supports, and crisis contacts.

Open handout →
Safety

Understanding Abuse

What abuse and coercive control are, why it’s not your fault, and that support exists.

Open handout →
Safety

Getting Help & Resources

Hotlines, what advocates do, online safety, planning ahead, and legal options.

Open handout →
Anxiety

Worry Management

Sort solvable worries from "what ifs," use worry time, and let the rest go.

Open handout →
Anxiety

Progressive Muscle Relaxation

A step-by-step tense-and-release sequence to drain physical tension.

Open handout →
Depression

Behavioral Activation & Scheduling

Act your way into feeling better with planned pleasure and mastery activities.

Open handout →
Depression

Mood Tracking & Monitoring

A daily 30-second log of mood, sleep, and triggers to spot patterns.

Open handout →
Self-Care

Self-Care Assessment & Plan

Rate how you're caring for yourself and pick one small change per area.

Open handout →
Self-Care

Stress Management & Burnout

Spot burnout early and rebalance demands against real recovery.

Open handout →
Relationships

Setting Healthy Boundaries

What boundaries are, why guilt is normal, and how to state them kindly.

Open handout →
Relationships

Assertive Communication

The middle path between bottling up and blowing up, using "I" statements.

Open handout →
Lifestyle

Diet & Exercise: The Basic Science

How movement and nutrition shape mood, energy, and the stress response.

Open handout →
Skills

SMART Goals & Committed Action

Turn values into specific, doable goals and follow through on tough days.

Open handout →
Anxiety

Grounding Techniques

Come back to the present with sensory, physical, mental, and soothing grounding.

Open handout →
Anxiety

Facing Fears: Exposure Hierarchies

Build a fear ladder and face avoided situations one manageable step at a time.

Open handout →
Self-Care

Healthy Habits & Gratitude

Anchor your day, stack small habits, and train attention toward the good.

Open handout →
Dementia
Dementia & Caregiving

Understanding Dementia

What dementia is, the main types, how it progresses, and what to expect.

Open handout →
Dementia & Caregiving

Communicating & Daily Care

Communication techniques, validation, and gentler daily-care routines.

Open handout →
Dementia & Caregiving

Managing Challenging Behaviors

The ABC approach for agitation, sundowning, wandering, and repetition.

Open handout →
Dementia & Caregiving

Home Safety Checklist

Fall prevention, wandering, medications, driving, and emergency readiness.

Open handout →
Dementia & Caregiving

Caregiver Stress & Self-Care

Recognize burnout, manage grief and guilt, and get real support.

Open handout →
Dementia & Caregiving

Planning Ahead: Legal & Care

Advance directives, powers of attorney, and care options and costs.

Open handout →
Dementia & Caregiving

Later Stages: Comfort & Grief

Advanced dementia, hospice and palliative care, and caregiver grief.

Open handout →
Substance Use
Alcohol

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.

Open handout →
Medications · Antidepressants
Antidepressant

SSRIs

How to take them, the under-25 warning, sexual and GI side effects, and what to watch for.

Open handout →
Antidepressant

SNRIs

Taking with food, blood-pressure monitoring, discontinuation, and serious side effects.

Open handout →
Antidepressant

Bupropion (Wellbutrin)

Activating, weight-neutral; the seizure risk, who should avoid it, and monitoring.

Open handout →
Antidepressant

Mirtazapine (Remeron)

Sleep and appetite, why low doses sedate more, and weight and lipid checks.

Open handout →
Antidepressant

Tricyclic Antidepressants

Overdose danger, heart effects, anticholinergic side effects, and EKG monitoring.

Open handout →
Antidepressant

MAO Inhibitors

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

Typical (1st-Gen) Antipsychotics

Movement side effects, tardive dyskinesia, the dementia warning, and AIMS/EKG checks.

Open handout →
Antipsychotic

Clozapine

Why it works when others don't, the required blood (ANC) monitoring, and heart and bowel warnings.

Open handout →
Medications · Mood Stabilizers
Mood Stabilizer

Lithium

Salt and fluids, toxicity signs, and blood-level, kidney, and thyroid monitoring.

Open handout →
Medications · Anticonvulsants
Anticonvulsant

Lamotrigine (Lamictal)

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 →

Chapters

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

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