The Psych Commute with Dr. Brown

#31 - DEAPL for making clinical decisions

In this episode of The Psych Commute, Dr. Brandon Brown introduces a practical clinical decision-making framework: DEAL and its more detailed version, DEAPL, designed for moments of uncertainty when time and information are limited. Using a tense inpatient case of a severely dysregulated patient with seizure-like activity in a resource-constrained psychiatric setting, he walks through how to systematically define the problem, enumerate options, assess whether you have enough information, predict possible outcomes, and ultimately choose the path that minimizes downside risk. The episode highlights how even in the absence of definitive diagnostics, structured thinking can guide safe, rational decisions and offers a mental model clinicians can carry into any challenging situation. This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit brandonbrownmd.substack.com [https://brandonbrownmd.substack.com?utm_medium=podcast&utm_campaign=CTA_1]

#30 Why I write my notes backward

I write my notes backward. Not in the traditional SOAP format (Subjective, Objective, Assessment, Plan), but essentially in reverse: Assessment & Plan → Data (Subjective + Objective) So instead of SOAP, it’s more like AP–SO. This format isn’t unheard of in medicine. It’s fairly common in internal medicine. But in psychiatry, it’s unusual enough that when colleagues cover for me, they sometimes copy my note forward and rearrange it back into standard SOAP. So clearly this is either misunderstood or mildly offensive to some people. Let me explain why I do it this way. At the very top of my note, I put a brief reason for admission: John Doe is a 56-year-old male with a history of schizophrenia and hypertension admitted for acute exacerbation of psychosis in the setting of medication non-adherence. 1. Running Hospital Course Next, I maintain a running hospital course, updated daily. I’ll structure it by hospital day: * Hospital Day 1: Admitted for psychosis. Started risperidone 1 mg BID and amlodipine 5 mg daily. * Hospital Day 2: Continued disorganization and auditory hallucinations. Increased risperidone to 1 mg AM / 2 mg PM. Just one or two sentences per day. Why? Because at discharge, I can copy this running course directly into the discharge summary. In Epic, there’s a built-in AI summarization tool that converts it into paragraph form. So I’m essentially writing my discharge summary in real time, a little bit each day. It saves me a ton of cognitive load at the end. Problem-Based Assessment and Plan After the hospital course, I move directly into a problem-based plan. Each problem gets its own header: # Auditory hallucinations / disorganized thought Under that: * Working diagnosis: Schizophrenia * If needed: Differential diagnosis * Workup (labs, studies) * Treatment plan If it’s straightforward, e.g. known schizophrenia with medication non-adherence, I keep it simple. If it’s undifferentiated, like: # Erratic behavior Then I’ll structure it more explicitly: * Working diagnosis: Psychosis unspecified * Differential: Substance-induced psychosis, schizophrenia, schizoaffective disorder, acute mania, encephalopathy * Workup: labs, UDS, imaging if indicated * Treatment plan If it’s complex, I’ll add some prose explaining my reasoning, for clarity and for liability purposes. But I generally don’t write long narrative assessment paragraphs the way many psychiatry notes do. The problem list always includes: * The primary psychiatric problem(s) * Medical comorbidities * Risk assessment and mitigation (suicide precautions, fall precautions, etc.) * Discharge planning And yes, I start thinking about discharge on day one. Are they going back to a shelter? A group home? Do we need a substance use referral? Guardianship? Long-acting injectable planning? That’s all part of the plan. Then Comes the Data Only after I’ve written the assessment and plan do I move to the data section. That includes: * Subjective * Objective * Labs * Vitals * Mental status exam * Physical exam To me, the subjective is just data. What the patient tells me is important, but it’s still data that feeds into the larger synthesis. I don’t start with a long narrative of what the patient said and then slowly build toward a conclusion. I already know what I’m treating and what decisions I’m making. The data supports that. Why This Works Better for Me 1. It Reflects How I Actually Think When I see a patient, I’m already forming an assessment and plan in real time. The note should reflect that. Starting with the plan forces clarity: * What are the actual problems? * What am I doing about them? * What’s the working diagnosis? * What needs workup? Once that’s clear, the subjective and objective sections become focused. I’m not transcribing everything the patient says. I’m documenting what’s relevant to the clinical questions I’m answering. It’s a filter. 2. It Improves Readability Let’s be honest: most people reading notes want to know the bottom line. If you’re covering me tomorrow, you don’t want to scroll through three paragraphs of subjective narrative to find the risperidone dose change. You want the assessment and plan. So I put it at the top. 3. It Keeps Me Focused When I’m writing multiple notes in a row, it gets tedious and I lose my attention especially when starting with the subjective. If I start with assessment and plan, I’m forced to: * Confirm diagnoses * Adjust meds * Update orders * Address risk issues * Think about discharge That’s the high-value work. Once that’s done, filling in the data is relatively mechanical. It also helps me avoid missing order changes. Writing the plan first sometimes reminds me of something I forgot to put in. A Simple Template Here’s a simplified version of what this looks like in practice. Reason for Admission 56-year-old male with schizophrenia and hypertension brought in by police for erratic behavior in public in the setting of medication non-adherence. Running Hospital Course * HD1: Admitted for erratic behavior, appears to be psychosis whether primary or secondary. Started risperidone 1 mg BID. Continued amlodipine 5 mg home med for HTN. * HD2: Persistent AH and disorganization. Increased risperidone to 1 mg AM / 2 mg PM. Assessment & Plan # Erratic behavior * Working diagnosis: Psychosis, unspecified * Differential: Substance-induced psychosis (UDS+ for cocaine), schizophrenia, schizoaffective disorder, mania, delirium, medical cause * Workup: CBC, CMP, TSH, UDS * Treatment: * Risperidone 1 mg AM / 2 mg PM * Monitor EPS, prolactin * Consider LAI prior to discharge # Hypertension * Continue amlodipine 5 mg daily # Risk Assessment / Mitigation * Suicide precautions: Q15 checks # Discharge Planning * Anticipated discharge to group home * Coordinate outpatient psychiatry follow-up * Evaluate for LAI prior to discharge Data (abbreviated) Subjective Patient reports ongoing voices commenting on behavior. Denies SI/HI. Reports poor sleep. Objective * Vitals stable * Labs pending * MSE: Disorganized thought process, AH present, insight limited * PE: No rigidity in UE This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit brandonbrownmd.substack.com [https://brandonbrownmd.substack.com?utm_medium=podcast&utm_campaign=CTA_1]

#29 Simulated Case: Altered Mental Status

On this episode of The Psych Commute, we try something a quite different. Instead of discussing a random idea as I drive home as usual, we run a fully simulated inpatient consult using AI voice actors (but I wrote the script with no AI involvement). The patient: a 65-year-old nursing home resident with schizophrenia sent to the ED for “altered mental status.” The workup is normal. The ED thinks it’s psychiatric. From there, things start to get complicated. This episode focuses much less on interview technique and much more on clinical reasoning and management. I’m experimenting with this format, so I’d genuinely like to know if it’s useful, useless, or somewhere in between. This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit brandonbrownmd.substack.com [https://brandonbrownmd.substack.com?utm_medium=podcast&utm_campaign=CTA_1]

#28 Mapping Mental Illness in Genetic Space

Mapping Psychiatric Disorders with GWAS I wanted to write record a brief episode about a paper I just read that came out in December 2025. The title is Mapping the genetic landscape across fourteen psychiatric disorders [https://www.nature.com/articles/s41586-025-09820-3] published in Nature. At a high level, this was a genome-wide association study (GWAS) looking across a large number of psychiatric diagnoses. The basic goal was to identify genetic variants that are correlated with different psychiatric disorders, and then see whether those disorders naturally cluster together in “genetic space.” They looked at fourteen psychiatric disorders, spanning both childhood-onset and adult-onset conditions, using a very large sample of over a million cases. The authors examined which alleles, particularly single nucleotide polymorphisms (SNPs), were most strongly associated with each diagnosis. Brief review of GWAS The goal of GWAS is to find genetic variants that are significantly more frequent in a particular condition compared to a control. Usually researchers are looking at variants in genes called single nucleotide polymorphisms or SNPs (pronounced snips), where a single DNA letter is different between different people, which could be enough to change the function of the gene. Most individual variants have very small effects, but when you look across many of them at once, patterns can emerge. GWAS is essentially a very large, statistical pattern-matching exercise across the genome. The five genetic clusters So the researchers did a big analysis on these over a million cases to discover SNPs that were more common in these disorders compared to controls, and then asked whether these variants clustered in meaningful ways across diagnoses. For example, they might find that a SNP on gene X was more frequent in schizophrenia than controls, but is also found more commonly in bipolar disorder cases. So then by looking at which disorders shared a lot of these SNPs they could cluster them together. What they found were five broad factors, where disorders within each factor shared a high degree of genetic overlap. The first factor was labeled SB, standing for schizophrenia and bipolar disorder. That factor included diagnoses of schizophrenia and bipolar disorder grouped together. They also identified an internalizing factor. In psychiatric and psychological research, internalizing generally refers to patterns like negative affect, rumination, self-criticism, and inwardly directed distress. This is often contrasted with externalizing, which involves outwardly directed behaviors like impulsivity, aggression, or blaming others. A third factor was a compulsive factor, which included diagnoses such as OCD, Tourette syndrome, and anorexia. The fourth was a neurodevelopmental factor, including diagnoses like autism. The final factor was a substance use disorder factor, which included most of the specific substance use disorders such as cannabis use disorder, stimulant use disorder, nicotine use disorder, and so on. The p-factor On top of these five factors, the authors also used a hierarchical model with a single node at the very top, which they called the p-factor. This idea isn’t new and has appeared in prior work. The p-factor represents genetic variants that seem to be shared across all psychiatric disorders, regardless of which specific cluster they fall into. So the structure looks something like this: a general p-factor at the top, five broad factors underneath it, and then individual diagnoses within each factor. Some genetic variants correlate broadly on all these tested disorders, while others are more specific to one factor. What do the genes actually do? The authors then asked a natural next question: what do these genes actually do, biologically? What kinds of proteins do they encode, and what processes are they involved in? Some of the findings were, in a way, reassuringly obvious. The substance use disorder factor, for example, included genes like alcohol dehydrogenase, which is directly involved in ethanol metabolism. There was also a SNP in a nicotinic receptor subunit. That fits common sense. Some people drink alcohol and feel terrible; they get no pleasure, and instead maybe some nausea or flushing. And people are unlikely to become addicted to something that feels bad. Other people find alcohol calming or even euphoric, which makes repeated use and addiction more likely. Differences in metabolism or receptor binding could plausibly contribute to that. Beyond substance use disorders, the findings were less straightforward. For the p-factor, the shared genes tended to be involved in very general biological processes, such as gene regulation. Nothing particularly specific or mechanistic stood out. For the schizophrenia-bipolar (SB) factor, there were genes involved in neuronal development, particularly excitatory neurons. The internalizing factor also showed some involvement of excitatory neuron genes, but the signal was less consistent. And for the compulsive factor, there wasn’t anything especially compelling in terms of functional interpretation. What does this mean for the DSM? One way to interpret these results is that the DSM may be splitting diagnoses too finely, drawing artificial boundaries between disorders that are not well supported biologically. Clinically, we already see this problem. At a single point in time, it can be genuinely difficult, or impossible, to distinguish bipolar disorder with psychosis from schizophrenia. The shared genetic signal between those diagnoses has been described before, and this paper reinforces that overlap. It naturally raises the question of whether these are truly distinct disorders, or whether they are different presentations of the same underlying condition. On the other hand, there’s an important limitation here. Psychiatric diagnoses are not static. People’s diagnoses change over time. Many clinicians have seen patients move from a bipolar diagnosis to schizophrenia, and then later back to bipolar disorder depending on who evaluates them and at what point in their illness. That diagnostic uncertainty inevitably contaminates genetic studies like this. It doesn’t invalidate the findings, but it likely distorts them to some degree. There’s one more point I’d emphasize. While there are clearly genetic risk factors for psychiatric conditions, I don’t think we’re going to find all the answers at the level of genes alone. If you think of the brain loosely as an information-processing system, an analogy that is not perfect, but still useful, consider this: take a very large, complex software program like Adobe Photoshop or Microsoft Excel that has millions of lines of code. Now run a million identical copies of that program on different computers. Some percentage of those programs will crash or behave unexpectedly. And the code is identical in every case. The failures happen because users push the software into regimes the original programmers didn’t anticipate. If you ran a GWAS on that situation, you wouldn’t learn much from the “code,” because the code is the same everywhere, even though failures still occur. I think something similar applies to psychiatric disorders. Genetics matter and may reveal some mechanistic vulnerabilities, but even genetically “normal” brains can experience psychiatric disorders when put in unexpected or extreme environments. So we shouldn’t expect gene-level analyses to give us a complete explanation of psychiatric illness. This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit brandonbrownmd.substack.com [https://brandonbrownmd.substack.com?utm_medium=podcast&utm_campaign=CTA_1]

#28 How I do my rounds for inpatient psych

I’ve worked in very high-volume settings. In a prior job, I did moonlighting where I would round on thirty-something patients per day, sometimes with ten or more admissions in a single day. Efficiency mattered a lot there, because otherwise you simply could not get through the work. I don’t recommend that kind of volume, by the way. Fortunately, academic medicine is more reasonable. I’m capped at twelve patients and have excellent social work assistance. What I want to focus on here are a few different rounding models I’ve tried, what’s worked for me, and a couple of simple frameworks I use regularly to stay systematic. I’ve tried three rounding models. The most common rounding model in my experience as a medical student and resident is where you show up in the morning, do a little pre-charting either that morning or the night before, then have a brief meeting where you get a nursing report. After that, you print your patient list and start seeing patients one by one. You might jot notes on your printout or try to keep everything in your head. Once you’ve seen everyone, you go back, put in consults, orders, and then spend the rest of the day writing notes and dealing with fires as they come up. I still do this sometimes. The problem for me is that I get very burned out writing twelve or more notes in a row. I lose focus quickly, it feels painful, and it’s not how I do my best work. The second model is seeing each patient one by one and finishing everything for that patient before moving on. That means seeing the patient, writing the note, putting in orders, and addressing whatever needs to be addressed right then. If the patient is calm enough, I’ll bring them into a room with a computer and type while we talk. If not, I’ll do it immediately afterward. This has actually become my preferred way of rounding. It does mean that I may not finish seeing patients until early afternoon, whereas with the first model you can often finish seeing everyone before lunch. But once I’m done, I’m done. Notes are in. Orders are in. There’s no looming pile of documentation waiting for me. Psychologically, that makes a big difference. There’s also a mixed model, which is probably my second favorite. In this approach, you do deeper pre-charting in the morning. You prep most of each note ahead of time, often everything except the subjective section. Based on the nursing report and the patient’s trajectory, you usually already know what you’re going to do with medications and orders, so you can often update those in advance as well. Then you round on all your patients. You still have notes to finish afterward, but much less work per note. My least favorite model is seeing everyone in the morning and then doing all the notes afterward. On one hand, it feels good to say you’ve seen all your patients. In a worst-case scenario, you can even finish notes at home. But for me, having a big block of notes waiting is draining and gets me burned out. A simple daily checklist: FLOP SEND Regardless of the rounding model, I try to be very systematic in how I approach each patient. I use a simple mnemonic I came up with called FLOP SEND. F is for flow sheets. In my EMR, that’s where vitals are recorded. I always check the most recent vitals and trends. Is my patient on clozapine becoming tachycardic? Is blood pressure creeping up? L is for labs. Are there any new results I need to act on? O is for orders. In my EMR, some orders are required to have an expiration date, so sometimes orders expire unintentionally. Consults fall off. Labs are due. I check that everything is current and put in new orders as needed. P is for problem list. I write problem-based notes, and it’s easy to forget things, especially chronic issues like hypertension, diabetes, and hypothyroidism. I make sure they’re all accounted for in my notes. S is for sleep. I think of sleep as a psychiatric vital sign. I always check how many hours the patient slept overnight. Minimal sleep is almost always something I need to address. Or sometimes hypersomnia is the problem. E is for events. Were there restraints, seclusion, emergency PRNs, or other significant overnight issues? N is for note. Just a checklist item to do my documentation. D is for discharge planning. I try to be thinking about discharge from day one. Where are they going? What aftercare will they have? How are we thinking about relapse prevention? They’re not necessarily in the perfect order, but as a checklist, FLOP SEND keeps me from missing the important things. A differential diagnosis framework: MINDSPACE The last thing I want to share is a mnemonic I use for differential diagnosis on the inpatient unit when seeing new admissions. It’s called MINDSPACE. When someone is admitted to inpatient psych for “erratic behavior” (a common presentation for me), there are a lot of possible explanations. MINDSPACE helps me stay systematic. M is for mania or manic-depression, what we now call bipolar spectrum disorders. I is for intoxicant, meaning substance-induced conditions, including intoxication and withdrawal. N is for neurodegenerative or acquired brain disease, such as dementia or traumatic brain injury. D is for (neuro)developmental conditions, like autism. S is for schizophrenia spectrum disorders. P is for personality disorders. A is for adjustment disorders, where something bad has happened and the patient is having a severe but understandable reaction. C is for catatonia. Catatonia is always secondary to something else, but it’s common enough on inpatient units that I want it explicitly on my differential so I don’t miss it. E is for encephalopathy. This is where orientation, memory, or attention are impaired, and where I need make sure the patient really was “medically cleared.” This framework isn’t perfect. No framework is. More than one thing can be going on at once. But as a quick mnemonic to avoid diagnostic premature closure, it helps. That’s it. I hope some of this is helpful to someone out there. This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit brandonbrownmd.substack.com [https://brandonbrownmd.substack.com?utm_medium=podcast&utm_campaign=CTA_1]