Lamotrigine toxicity may be associated with a variety of nonspecific clinical findings, and rarely with psychosis. Many previous studies have reported that the use of lamotrigine with other agents, such as valproic acid, or an overdose of lamotrigine precipitated symptoms of lamotrigine toxicity. This case involved a 31-year-old woman who experienced dizziness, emesis, and psychosis after her lamotrigine prescription had recently been increased. These symptoms resolved when lamotrigine was held after the diagnosis of lamotrigine toxicity had been made. To our knowledge, this is a rare documented case of psychosis associated with lamotrigine toxicity, independent of intentional overdose or concurrent use of valproic acid.

Serotonin syndrome (SS) is a rare but potentially life-threatening condition resulting from increased serotoninergic activity in the central nervous system, either from exposure to a serotonin agonist or from withdrawal of a serotonin antagonist. Clozapine withdrawal has been implicated in cases of serotonin syndrome; however, clozapine exerts both agonist and antagonist properties at the serotonin receptor. We present the case of a 37-year-old male with unspecified psychosis and a structural neurological deficit who developed SS according to the Hunter Criteria while on a regimen of clozapine, paliperidone, and prednisone taper. Within an hour of receiving 400 mg of clozapine, the patient developed fever, tachycardia, diaphoresis, tremor, hyperreflexia, and inducible clonus. His symptoms resolved with supportive care, including intravenous fluids, benzodiazepines, and acetaminophen. We speculate that clozapine exerted its serotoninergic properties to induce SS symptoms in our patient, although alternative considerations and etiologies are discussed. We also include a review of the literature on cases of serotonin syndrome associated with clozapine. Five case reports were identified, all of which described SS occurring in the context of clozapine withdrawal or discontinuation. To our knowledge, ours is the first case suggestive of clozapine-induced SS. This case highlights the importance of considering SS in patients receiving clozapine, especially when concomitant medications may amplify serotoninergic effects. In addition, clinicians should exercise caution when using clozapine in patients with complex neurological conditions or in those with atypical psychiatric presentations. Close monitoring is needed when clozapine dose adjustments are made.

Tens of millions of people are already using chatbots as psychotherapists. Many find them helpful, but some are gravely harmed. This column helps clinicians understand the long history of chatbots; why they have suddenly burst on the scene now; current indications and contraindications; future risks and benefits; and how to identify and treat chatbot-induced disorders. A hybrid model will likely become increasingly prevalent, with human clinicians and chatbots working together to synergize each other's strengths and cancel each other's weaknesses. Chatbots are rapidly infiltrating our field. Clinicians cannot afford to be complacent in learning to adapt to the rapidly changing mental health landscape.

Therapy-interfering behavior (TIB), although commonly encountered in clinical practice, often goes unaddressed. But if behaviors preventing treatment engagement are not addressed, patients will struggle to achieve their treatment goals, will remain at high chronic risk for suicide, and may drop out of treatment. Therefore, to truly help our patients approach their stated goals and target suicide risk, it is critical to address TIB. In this first column of a 2-part series, we discuss how to identify TIBs in both patients and providers to facilitate therapeutic risk management of patients at risk for suicide.

Psychiatry has long been considered a biopsychosocial discipline, but, in the age of evidence-based medicine, clinical care is becoming increasingly fragmented and manualized. We continue to separate "biological" and "psychological" modalities in spite of mounting evidence that psychotherapy has a direct impact on brain physiology, and that psychopharmacological treatments carry meaning that often determines its real-life effectiveness. Evidence-based treatments (EBTs) focus clinical attention on the patient's symptomatic presentation and functional capacity that define their generic DSM-5 diagnosis. Yet, understanding the person of our patients and their experience of the illness goes beyond static diagnostic labels and involves exploration of their unique subjective and relational dynamics. Therapeutic alliance, a major factor in the treatment outcome across both psychotherapeutic and psychopharmacological modalities, has become increasingly marginalized as more psychiatrists shift toward single consultation practices, where the full scope of the relational meaning is largely lost. Conversely, the minority of practitioners who continue to offer psychotherapy are often less familiar with psychopharmacological modalities. Although psychopharmacology and psychotherapy are both clinically effective, their outcomes and cost-effectiveness are further enhanced when they are applied in tandem, in the context of a nurturing relationship with the treatment provider. Below, we examine the limitations of the current EBT paradigm and the evidence for an individualized integrated wellness model that relies on empirically supported principles of care.

Psychopharmacology, once propelled by a series of serendipitous mid-20th-century discoveries, has matured into a field defined by mechanistic diversity, translational neuroscience, and an expanding array of circuit-based interventions. Despite more than 100 approved psychiatric drugs, remission rates for major depressive disorder and other serious mental disorders remain modest, underscoring the biological heterogeneity embedded within syndromic diagnoses. Roughly 60% of patients with major depressive disorder respond to monoaminergic treatments, while others respond preferentially to glutamatergic agents such as ketamine or esketamine, and a smaller subset remains minimally responsive to both. These differential response patterns challenge the notion of a singular depressive disorder and highlight the need for biologically informed patient stratification. Contemporary psychopharmacology extends well beyond classic neurotransmitter modulation, encompassing synaptic plasticity, circuit regulation, inflammatory pathways, neurosteroids, muscarinic systems, drug-assisted psychotherapies, and computational neuroscience. Parallel advances in neuromodulation, including repetitive transcranial magnetic stimulation, transcranial direct current stimulation, vagus nerve stimulation, focused ultrasound, and adaptive deep brain stimulation, reflect a shift from region-based to network-based conceptualizations of psychiatric illness. Simultaneously, advances in pharmacogenomics, neuroimaging, artificial intelligence, and biomarker identification are beginning to make precision psychiatry a practical, though still emerging, reality. With these broadly described advances in mind, this column reflects on the historical trajectory of psychopharmacology, explores the convergence of pharmacology and neuromodulation, and considers the future of psychiatry through the lens of mechanism-based and personalized care. In doing so, it aims to carry forward the disciplined, mechanistically grounded scholarship that has long characterized this column.

Syphilis, a condition known as "the great imitator," is a sexually transmitted infection caused by the bacterium Treponema pallidum that can present with a myriad of symptoms, including psychiatric and neurological changes. Severe complications of syphilis are rare nowadays due to the widespread availability of antibiotics. Nonetheless, the incidence has been increasing over the past few years. We describe the case of a middle-aged man who presented with neuropsychiatric symptoms that were initially thought to be secondary to substance use and who was eventually diagnosed with neurosyphilis. A brief review of the most common features of this condition, as well as treatment options, is presented. As this patient was part of a minority group and had a history of substance misuse that delayed the diagnosis of neurosyphilis, we will also comment on stigmas, disparities, and biases in clinical settings, and some mitigation strategies that can be implemented to prevent adverse health outcomes in marginalized populations.

Frontotemporal dementia (FTD) and Lewy body dementia (LBD) are distinct neurodegenerative disorders that rarely co-occur. However, their overlapping features can obscure diagnosis and complicate management. We present the case of a 65-year-old man with a history of alcohol use disorder, diabetes, and blindness who developed acute behavioral changes, catatonia, and fluctuating mental status. He exhibited signs consistent with a behavioral variant FTD, including disinhibition, executive dysfunction, and hypersexuality, as well as features associated with LBD, including visual hallucinations, autonomic instability, and waxing-and-waning impairment in cognition. His hospital course was marked by episodic disorientation, variable language use, and persecutory delusions. Neuroimaging, cerebrospinal fluid analysis, and serial neuropsychological testing yielded mixed and inconclusive results, contributing to the diagnostic ambiguity. Treatment included lorazepam, which improved catatonic symptoms but was discontinued due to risk of delirium, and aripiprazole, which was tapered due to suspected neuroleptic sensitivity. The patient was ultimately discharged to memory care with a diagnosis of an unspecified dementia. This case underscores the challenges of diagnosing and managing patients with overlapping features of multiple neurodegenerative disorders. Recognizing points of overlap between syndromes like FTD and LBD is key to tailoring interventions and avoiding harm. Serial cognitive assessments, functional neuroimaging, and biomarker analysis may improve diagnostic accuracy, although these tools have limitations. A deeper understanding of the pathophysiology of overlapping dementia syndromes is crucial for improving diagnostic clarity and guiding treatment strategies.

The rapid adoption of social media and now artificial intelligence (AI)-based chatbots has outpaced formal clinical guidelines on their use. Cases of alleged harm from both social media and AI use have accumulated in 2026. The recent Meta social media verdict hinged on a clinical question answered outside the clinical context. A similar pattern is repeating with AI, where litigation is moving faster than psychiatric consensus and even the pace of technological change. Assessing the risks and benefits of AI is thus critical but remains challenging, as harms may vary across rapidly evolving models, and benefits can change as well. Thus, clinicians need to be well informed about AI, and we present a framework for clinician competency in AI, including fundamentals of how AI is trained, how to ask about patient uses, and how to evaluate for risky engagement. We also propose using a familiar approach, the biopsychosocial formulation, to document and conceptualize AI use within a patient's life for a more nuanced assessment. With this discussion, we inaugurate the Digital Psychiatry column in the Journal of Psychiatric Practice and welcome submissions on the intersection of technology and mental health.