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

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#30 Why I write my notes backward

Feb 1800:07:54Tap to summarize

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 CourseNext, 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 PlanAfter the hospital course, I move directly into a problem-based plan.Each problem gets its own header:# Auditory hallucinations / disorganized thoughtUnder that:* Working diagnosis: Schizophrenia* If needed: Differential diagnosis* Workup (labs, studies)* Treatment planIf it’s straightforward, e.g. known schizophrenia with medication non-adherence, I keep it simple.If it’s undifferentiated, like:# Erratic behaviorThen 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 planIf 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 planningAnd 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 DataOnly 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 examTo 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 Me1. It Reflects How I Actually ThinkWhen 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 ReadabilityLet’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 FocusedWhen 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 dischargeThat’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 TemplateHere’s a simplified version of what this looks like in practice.Reason for Admission56-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 dischargeData (abbreviated)SubjectivePatient 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

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#29 Simulated Case: Altered Mental Status

Feb 1700:12:18Tap to summarize

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

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#28 Mapping Mental Illness in Genetic Space

Feb 900:09:44Tap to summarize

Mapping Psychiatric Disorders with GWASI 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 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 GWASThe 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 clustersSo 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-factorOn 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

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#28 How I do my rounds for inpatient psych

Feb 500:09:20Tap to summarize

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 SENDRegardless 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: MINDSPACEThe 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

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#27 Focused Ultrasound in Psychiatry

Jan 3100:11:31Tap to summarize

I want to talk about focused ultrasound and its potential role in psychiatry. Right now, it is not an established psychiatric treatment, but it is being actively studied and I think there is a good chance it becomes part of our clinical toolkit in the next several years (albeit perhaps only at academic centers initially). Small clinical trials are already underway, and the technology itself is further along than many people realize.Let me start with the basics.Most of us are familiar with diagnostic ultrasound, where sound waves are sent into tissue and the reflected signals are used to build an image of internal structures. With focused ultrasound the goal is to concentrate ultrasound energy at a specific point in the brain. Once you can reliably focus that energy, you can either modulate neural activity at that point or, at higher intensities, create a lesion by heating and destroying tissue.Broadly speaking, there are two categories people talk about: low intensity focused ultrasound, often called LIFU, and high intensity focused ultrasound, or HIFU. There is not a universally agreed upon cutoff that separates the two. Some papers mention specific power levels like 100 watts as the boundary, but in practice the distinction is really about intent and biological effect. LIFU aims for reversible neuromodulation without permanent tissue damage. HIFU is used when the goal is thermal ablation and permanent lesioning.The reason I am especially interested in LIFU is that it may address some of the inherent limitations of TMS. TMS is a great tool, but it has an inherent physical tradeoff between depth and focality. The deeper you try to stimulate, the less focal the stimulation becomes. If we want to target specific circuits, focality matters a lot. With TMS, once you move beyond superficial cortex, you quickly lose precision.Focused ultrasound has the theoretical advantage of reaching deep brain structures while still maintaining millimeter scale focality. The exact focal size depends on a number of factors, including frequency and skull properties, but in general it can be more precise at depth than what we can do with standard TMS.One of the most interesting aspects of LIFU is that it can modulate neural activity without causing lesions. Interestingly, the exact mechanism for this is not known. Ultrasound is fundamentally a mechanical pressure wave, so the question becomes how mechanical energy influences neurons. There is evidence that mechanosensitive ion channels play a role. For example, certain potassium channels located at the nodes of Ranvier appear to respond to mechanical forces, which could alter neuronal excitability. That said, this is still an active area of research and there are likely multiple mechanisms involved.Depending on the stimulation parameters, LIFU has been shown to either enhance or suppress neural activity. Pulse duration, frequency, and intensity all matter. Many studies have demonstrated inhibitory effects, almost like creating a temporary functional lesion, but excitatory effects have also been reported. At this stage, the field is still mapping out which parameters reliably produce which outcomes.There is also a fascinating physics angle when focused ultrasound is used inside a strong magnetic field, such as in an MRI scanner. In that setting, the motion of charged particles induced by ultrasound can interact with the magnetic field to produce a small electrical effect. In simple terms, ultrasound physically moves ions, and in the presence of a magnetic field that motion can be converted into an electrical influence on neurons. This concept is sometimes referred to as transcranial magneto acoustic stimulation. A brief dive into the physics is worth it. The key idea comes from something called the Lorentz force, which describes how charged particles behave in electric and magnetic fields.F = q(E + v × B)F is the Lorentz force, which in this context is the force acting on a charged particleq is the charge of the particle (e.g. could be +1 or -1 or 0)E is the electric fieldv is the velocity of the charged particleB is the magnetic fieldYou do not need to follow the math in detail, but the equation gives us some helpful intuition if you just pay attention to cases where the force is 0 vs non-zero. If there is no charge, there is no force. If there is no electric field and no motion, there is no force. But if charged particles are moving in the presence of a magnetic field, they will experience a force, even in the absence of an electric field.In neurons, the charged particles are ions. In a strong magnetic field like an MRI scanner, there is usually no meaningful electric field being applied. But if we use ultrasound, we are physically moving those ions back and forth. That motion in the magnetic field can generate tiny forces on the ions, leading to local and small electrical effects. In other words, mechanical energy from ultrasound can be converted into electrical influences on neural tissue.The takeaway is that focused ultrasound in a magnetic field may offer a way to modulate neural activity through both mechanical and electrical mechanisms, which is part of what makes this technology so intriguing.It is not yet a clinical tool, but it highlights how versatile this technology might become.Another promising application of focused ultrasound is temporarily opening the blood brain barrier. When ultrasound is applied alongside microbubbles, it can safely and transiently increase the permeability of blood vessels in targeted brain regions. This allows medications that normally do not cross the blood brain barrier to enter the brain more easily. This approach is being actively studied in humans, especially in brain tumor treatment, though it is still largely investigational rather than standard clinical practice. There is also experimental work looking at targeted drug delivery where ultrasound helps release medications in specific regions, which could eventually have psychiatric applications.High intensity focused ultrasound is already in clinical use for certain neurological conditions. The most established example is the treatment of medication refractory essential tremor. In this case, focused ultrasound is used to create a small lesion in a specific thalamic target, typically the ventral intermediate nucleus. This is done with MRI guidance, and one of the remarkable features is that temperature can be monitored in real time using MRI thermometry. The tissue is gradually heated into a range that produces thermal ablation, usually in the mid to high 50s Celsius, while carefully observing both imaging and clinical effects.There has also been research using focused ultrasound lesioning for severe, treatment refractory psychiatric conditions. For example, capsulotomy targeting the anterior limb of the internal capsule has been studied in obsessive compulsive disorder and, to a lesser extent, major depressive disorder. These are small studies so far, but they are part of a broader resurgence of interest in carefully targeted neurosurgical interventions for psychiatric illness (“psychosurgery”).One practical limitation of focused ultrasound is skull anatomy. The skull can distort and absorb ultrasound energy, and not everyone is an ideal candidate. A measure called skull density ratio is often used to estimate how well ultrasound will transmit. Depending on specific intervention, roughly twenty percent of patients may not reach therapeutic temperatures with current technology for HIFU.Overall, I am very excited about focused ultrasound being used for psychiatric purposes. Focused ultrasound offers a combination of depth, focality, and flexibility that is hard to achieve with other noninvasive techniques. There is still a great deal we need to learn about optimal parameters, mechanisms of action, and long term safety. For now, it is something worth keeping an eye on. 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

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#26 ECT for PTSD

Jan 2900:07:10Tap to summarize

Electroconvulsive therapy (ECT) is not FDA-approved for post-traumatic stress disorder (PTSD), and it doesn’t have an established clinical indication for PTSD in the way it does for severe depression, mania, catatonia, or treatment-resistant psychotic disorders. That said, over the past several years there has been mounting evidence suggesting that ECT may be helpful for some patients with particularly severe PTSD, especially when comorbid with major depression.There have been a few recent meta-analyses showing a beneficial signal. One open question is whether this effect is simply due to ECT treating comorbid depression, with downstream improvements in PTSD symptom scales, or whether ECT is directly affecting core PTSD pathology itself. That question isn’t settled. But many clinicians, myself included, suspect that there may be a more direct effect.Part of that suspicion comes from clinical experience. I’ve treated patients where the primary indication for ECT was major depression, but who also had severe, comorbid PTSD. In a few cases, patients told me something interesting: ECT didn’t help their depression very much, but it substantially improved their PTSD symptoms. They felt less anxious, less hypervigilant, and less easily triggered. For them, the main reason to continue ECT wasn’t mood improvement, it was relief from PTSD symptoms.At first, these were unusual isolated cases. But as I became more aware of the broader case literature, it started to feel less anomalous and more like a real signal worth taking seriously.So how could ECT plausibly help PTSD?At a very basic level, ECT is a highly non-specific brain intervention. You are passing an electrical current through large swaths of brain tissue and inducing a generalized tonic-clonic seizure. We know ECT affects synaptic plasticity and appears to stimulate neurogenesis in certain regions, particularly the hippocampus. Given how non-specific its effects are, it wouldn’t be surprising if ECT also modulates circuits involved in PTSD, including amygdala-centered threat and fear networks.This kind of non-specificity is actually the norm in psychiatry. Many of our treatments affect multiple circuits at once, which is why the same medications and interventions often work across diagnostic categories. One core feature of PTSD is overlearning or overgeneralization. A traumatic event becomes decoupled from its original context and generalized far beyond where it should apply. For example, a combat veteran who experienced an IED explosion may later experience intense fear responses in entirely different settings, back home, years later, triggered by something like fireworks. The brain has failed to properly contextualize the trauma as something that occurred in a specific time and place.That’s essentially a failure of contextual learning. Because the hippocampus plays a key role in contextualization, one speculative idea is that ECT’s effects on hippocampal plasticity might help loosen this pathological overgeneralization. This is admittedly a hand-wavy explanation, but it’s at least biologically plausible.Another mechanism that feels more immediately compelling to me involves the autonomic nervous system.During a typical ECT treatment, there is a characteristic triphasic autonomic response. First, there is parasympathetic activation, which can cause bradycardia or even brief asystole. That is followed by a sympathetic surge with transient but often marked hypertension and tachycardia. Finally, there is a return of parasympathetic activity that brings the system back toward baseline.Over the course of an ECT series, the brain adapts. Seizure threshold increases, and autonomic recovery tends to become faster. Clinically, this looks like the sympathetic surge shutting off more quickly and the parasympathetic system reasserting control sooner.PTSD is strongly associated with autonomic hyperactivation, particularly excessive sympathetic tone. If ECT enhances the nervous system’s ability to down-regulate sympathetic activation and restore parasympathetic balance, that could directly target a core physiological component of PTSD. This idea also aligns conceptually with other investigational PTSD treatments that target autonomic regulation, such as stellate ganglion block.There’s also a more indirect but important possibility: ECT may improve overall cognitive flexibility. If that’s the case, it could make patients more able to engage in and benefit from psychotherapy, which remains the most effective treatment modality for PTSD. In that sense, ECT wouldn’t be replacing psychotherapy, but potentially enabling it.So while ECT is not a first-line or standard treatment for PTSD, there is growing evidence, and plausible biology, suggesting it can be useful in severe cases, particularly when comorbid depression is present. At minimum, it’s something worth keeping in mind and discussing thoughtfully with patients when conventional approaches haven’t been enough. 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

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#25 External combined nerve stimulator for depression, now approved

Jan 2800:10:31Tap to summarize

I recently read the randomized controlled trial for a new neuromodulation device called ProlivRX. It’s an external nerve stimulator that is now FDA approved for major depressive disorder in patients who are already on antidepressants and haven’t benefited from them.This comes on the heels of the recent FDA approval of the Flow Neuroscience FLX-100 transcranial direct current stimulation (tDCS) device for depression. It’s interesting that we’re seeing multiple new neuromodulation devices entering the space at the same time, and that both are home-based treatments.The randomized controlled trial was reasonably sized with 124 patients total. It was a blinded, sham-controlled, multi-site trial, and it was industry sponsored by the device manufacturer, NeuroLief, an Israeli company.The device stimulates branches of the trigeminal nerve along the forehead as well as occipital nerve branches at the back of the head. There has actually been another trigeminal nerve stimulation device that was FDA cleared for ADHD in the past. A more recent randomized controlled trial of trigeminal nerve stimulation for ADHD in children and adolescents was negative, it did not show benefit over placebo.In this trial, the authors point to studies suggesting that stimulating these nerves can affect brain circuits involved in mood regulation and attention networks. At some level, everything in the brain is connected, so stimulating one peripheral input is going to have downstream effects somewhere else. I’m not particularly impressed by that line of reasoning on its own, but it provides the rationale for why they tested this approach. Their specific hypothesis was that combining trigeminal and occipital nerve stimulation might be synergistic.The currents used in this trial were quite high compared to tDCS. Typical tDCS uses about 1–2 milliamps, whereas this device used currents in the range of roughly 6–18 milliamps. That’s a substantial difference, and it would definitely be noticeable to the patient. That said, the electrodes are spaced much closer together and the current is passing through superficial tissue rather than through the skull, as in tDCS. The device also uses a biphasic alternating current rather than direct current, so the electrical properties are quite different overall.The sham condition involved stimulation at a much lower current amplitude and lower frequency. Based on their blinding integrity testing, the blind mostly held. About 14% of participants in the active group correctly guessed they were receiving active treatment, and about 6% in the sham group correctly guessed they were in the sham condition. The authors modeled the effects of this partial unblinding and concluded that it did not meaningfully alter the primary outcome.The primary result was a statistically significant effect. The active treatment group had about an 8-point reduction on the Hamilton Depression Rating Scale, compared to about a 6-point reduction in the sham group. That works out to roughly a 2.6-point difference between groups. This translated into an effect size of around 0.7 to 0.8, which is surprisingly large given the relatively small absolute difference on the Hamilton scale.Effect sizes, of course, depend heavily on variability. My suspicion is that the trial design intentionally limited variability, shrinking the denominator in the effect size calculation and inflating the apparent magnitude. I’ll probably write more about this in the future, because this is a general issue with how effect sizes are interpreted. For context, typical SSRI trials show effect sizes around 0.3–0.4, so an effect size approaching 0.8 stands out—especially in a population that includes patients who have already failed antidepressant treatment. I can’t recall whether all participants met strict criteria for treatment-resistant depression, but at least a subset had failed two or more antidepressant trials.If you look at remission rates, the results are more modest. Remission was on the order of 20–30%, with somewhat higher response rates. Still, if those numbers hold up, a roughly 20% remission rate for a relatively benign, home-based treatment may be meaningful for some patients.The randomized portion of the trial lasted eight weeks, which is when the primary outcome was assessed. After that, the study continued in an open-label phase for an additional sixteen weeks. Once participants were unblinded, they continued treatment and showed incremental improvement over that longer period, which is encouraging.The treatment protocol involved using the device for 40 minutes at a time, twice daily, five to seven days per week.There were essentially no major device-related adverse events reported.So what do we make of all this? I’ve already hinted at some skepticism. Most psychiatric treatments—whether medications, ECT, or neuromodulation—do fairly nonspecific things. That’s likely why many treatments have efficacy across multiple diagnoses that probably involve very different underlying mechanisms. The brain is deeply interconnected, and almost any intervention will have widespread effects.This was an industry-sponsored trial, and while the authors offer putative mechanisms, the true mechanism is no clearer than it is for most psychiatric interventions. In terms of mechanism, the neuromodulation modality where we have the most hypothesis-driven, model-based understanding is probably TMS, where focal stimulation and functional imaging allow for more direct testing of circuit-level theories.Another important point is timing. The primary outcome wasn’t reached until week eight, with further gradual improvement afterward. This is not an acute treatment for severe or urgent depression. For someone who is severely ill or needs rapid symptom relief, options like ketamine, ECT, or aggressively titrated medications are likely more appropriate.That said, for patients with lower-urgency depression who are well resourced and can afford a device like this, it may be reasonable to try. If I were choosing between this device and a home-based tDCS device, I would personally lean toward tDCS, simply because there is a much larger research literature and somewhat more confidence about the circuits being targeted. Still, this appears to be a relatively harmless intervention. The worst-case scenario is mostly lost time and money.For low-urgency depression, it’s worth considering. And, as always, it’s helpful to have more tools in the toolkit. 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

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#24 The First Non-Antipsychotic Antipsychotic

Jan 2400:12:46Tap to summarize

In this episode, I break down one of the most interesting new developments in schizophrenia treatment: a medication that treats psychosis without dopamine blockade. And it also works for negative symptoms.I’m talking about xanomeline–trospium, brand name Cobenfy, a muscarinic-based therapy that targets M1 and M4 receptors, avoids extrapyramidal symptoms and metabolic side effects, and is not technically classified as an antipsychotic by the FDA. I walk through the mechanism, the EMERGENT trial data, efficacy for both positive and negative symptoms, side effect profile, dosing pearls, and where this might fit clinically. 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

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#23 Let's stop talking about neurotransmitters

Jan 2100:09:24Tap to summarize

We spend a lot of time explaining psychiatric medications in terms of neurotransmitters and receptors, but that may be the wrong level of abstraction. In this episode, I argue that psychiatric illness is better understood as a problem of brain circuits and information processing, not low-level mechanisms like receptors, and that this helps explain why treatments like ECT and clozapine work when others don’t. We should instead investigate how medications affect actual brain functioning at a circuit-level, and to do that we will have to think beyond neurotransmitters. 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

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All episodes

#31 - DEAPL for making clinical decisions

#30 Why I write my notes backward

#29 Simulated Case: Altered Mental Status

#28 Mapping Mental Illness in Genetic Space

#28 How I do my rounds for inpatient psych

#27 Focused Ultrasound in Psychiatry

#26 ECT for PTSD

#25 External combined nerve stimulator for depression, now approved

#24 The First Non-Antipsychotic Antipsychotic

#23 Let's stop talking about neurotransmitters