I give a full start-to-finish overview of how electroconvulsive therapy is delivered in real clinical practice. In the prior ECT episode, I focused on key concepts in ECT. Here, I zoom out and walk through the actual workflow: consultation, medical clearance, informed consent, anesthesia, seizure monitoring, and post-procedure recovery.

I begin at the referral stage: how an ECT psychiatrist evaluates whether a patient has an ECT-responsive condition (severe unipolar depression, bipolar depression, mania, or catatonia), and how we assess medical risk. I explain what “pre-procedural clearance” really entails, when internal medicine is involved, and how risk tolerance differs between freestanding psychiatric hospitals and full medical centers.

From there, I describe what patients can expect during the consult visit: medical review, physical exam, basic labs, EKG, optional chest X-ray, and baseline cognitive screening such as a MOCA or MMSE. I explain why documenting cognition before treatment is clinically important and offers medicolegal protection later if questions arise.

Next, I walk through the procedural day itself:

* patient check-in and nursing assessment

* IV placement and pre-anesthesia review

* EEG lead placement and cardiac monitoring

* the procedural “timeout”

* induction with methohexital and paralysis with succinylcholine

* controlled bag-mask ventilation with hyperventilation (to lower seizure threshold)

I explain the logic behind the cuff technique, why we tourniquet the right ankle, and how it helps confirm both seizure generalization and adequate depth of anesthesia.

Finally, I describe how stimulus electrodes are applied, what the seizure looks like on motor and EEG channels, why the motor seizure ends before the EEG seizure, and what happens immediately afterward as patients emerge from anesthesia and transfer back to PACU.

Let me know what you think, leave a review. Or email me at [email protected]

In this first installment of the ECT series, I walk through the foundations of electroconvulsive therapy from the perspective of someone who practices it regularly in a busy clinical service. Despite decades of stigma and misunderstanding, ECT remains the most effective treatment in psychiatry for several severe and life-threatening conditions, and modern research has repeatedly demonstrated its safety.

I start with a brief history, from ECT’s origins in 1938, to how the modern procedure works: inducing a generalized tonic–clonic seizure under general anesthesia using a short electrical stimulus. I also review what we know from animal studies, neuroimaging, and post-mortem human data: there is no evidence that ECT causes brain damage. Instead, its side effects, especially anterograde and retrograde amnesia, appear to stem from neuroplastic changes rather than neuronal injury.

I then discuss the major indications for ECT:

* Severe unipolar and bipolar depression

* Psychotic depression

* Catatonia (one of the most dramatic responders)

* Acute exacerbations of schizophrenia or schizoaffective disorder

* Mania, though less commonly treated because manic patients often decline the procedure and involuntary ECT is rare.

I also explain why ECT is one of the safest procedures in medicine when performed properly. I describe the characteristic physiologic response: a brief parasympathetic surge during the stimulus (bradycardia or even a few seconds of asystole) immediately followed by a robust sympathetic surge during the seizure (often dramatic but transient increases in blood pressure and heart rate). I discuss when and how we pre-treat with labetalol, and why its mild anti-seizure effects require careful balancing.

Finally, I cover procedure-related complications and how we manage them: prolonged seizures, tardive seizures, anesthetic choices (methohexital, propofol, ketamine, etomidate), and the pros and cons of different paralytics such as succinylcholine and rocuronium with sugammadex.

Questions or comments? Email me at [email protected]

I take a closer look at treatment-resistant depression (TRD), what the term actually means, why it’s far less useful than people think, and how I approach severe depressive episodes in real practice.

Most definitions of TRD frame it as unipolar major depression without psychotic features that has failed to remit after two adequate trials of first-line antidepressants. But as I discuss in this episode, this “two-step failure” model doesn’t tell us anything meaningful about biology, prognosis, or subtype. It simply reflects that our first-line medications (SSRIs, SNRIs, bupropion, mirtazapine) are not particularly effective to begin with. Data from STAR*D and other large trials reinforce this problem: even responders have high relapse rates.

Instead of rigidly following algorithms designed around weak medications, I argue for a severity-based approach. On the inpatient unit, especially with suicidality or a recent suicide attempt, it often makes more sense to go directly to augmentation rather than waiting six weeks for an SSRI to maybe work. I talk through why agents like aripiprazole can produce meaningful clinical change within days, how I present options to patients, and why we should treat severe MDEs with the same urgency and multimodal strategy we routinely use for manic episodes.

We also cover the broader therapeutic landscape: lithium augmentation, switching antidepressants, TMS, ECT, IV ketamine, intranasal esketamine, and psychotherapy, plus why I’m particularly optimistic about accelerated neuromodulation protocols like SAINT and emerging one-day TMS approaches.

In this episode of Dr. Brown’s Psych Commute, I break down one of the most commonly missed syndromes in acute psychiatry: catatonia. Although many clinicians think of it as rare, catatonia occurs in roughly 10–20% of psychiatric inpatients, and in my day-to-day practice, that statistic holds up.

I walk through the clinical signs that often get overlooked, how to use the Bush–Francis Catatonia Rating Scale, and why a proper lorazepam (Ativan) challenge remains the fastest and most reliable diagnostic tool. We also cover IV vs IM vs PO dosing, the timelines for reassessment, and why lorazepam’s pharmacokinetics make it the best choice.

I also discuss how to titrate scheduled benzodiazepines, what “high-dose” really means in severe catatonia, and when it’s time to move to ECT. Patients with catatonia often respond dramatically to ECT within one to four treatments, a pattern very different from depressive indications.

Finally, I talk about the differential diagnosis of catatonia. I also highlight excited catatonia, which is frequently mistaken for secondary agitation. Let me know what you think at [email protected].

In this short introductory episode, I share what this new psychiatry podcast is all about and why I’m starting it. I’m Dr. Brandon Lee Brown, an inpatient psychiatrist in Houston with a background spanning outpatient and inpatient care, interventional psychiatry (TMS, IV ketamine, intranasal esketamine, ECT), and psychotherapy.

My goal is simple: to record brief, high-yield reflections during my commute to or from work, covering cases, clinical patterns, and lessons I wish someone had told me when I was a trainee. Episodes will focus primarily on psychiatry, but will often touch on medicine more generally, neuropsychiatry, and the broader brain sciences.

I’ll discuss real issues that come up on the unit, interesting clinical dilemmas, and ideas from the papers and books I’m reading. Whether you’re a psychiatrist, resident, medical student, or someone who wants to know more about the practice of psychiatry, this podcast is designed to be practical, candid, and grounded in daily clinical work.

If you have questions or topics you’d like me to cover,you can reach me at [email protected].