Tardive dyskinesia is a disturbance in the balance between dopamine receptor stimulation and dopamine receptor blockade in the motor striatum, with hypothetically too much stimulation of supersensitive D2 receptors, resulting in “don’t stop” signaling to motor output.

Unravelling the mystery of dopamine neurotransmission, especially at its 3 most clinically relevant receptors, D3, D2, and D1, helps explain the pathophysiology of numerous psychiatric and neurologic symptoms in various CNS disorders that are theoretically caused by dysregulation of this neurotransmitter.

Drugs for psychosis and mood that bind dopamine D2 receptors can be classified not only by whether they also block serotonin 2A receptors, but by whether they also bind D3 or D1 receptors.

The classical point of view—that major depressive episodes (MDEs), no matter what additional symptoms are present, should be treated first line with antidepressants—is now giving way to new a notion. The idea is that MDEs mixed with a few symptoms of mania/hypomania should be viewed very differently in terms of their natural history, clinical outcome, and treatment, and perhaps certain antipsychotics should be given as first-line treatment rather than antidepressant monotherapy.

Migraine varies in its frequency, severity, and impact; treatment should consider these variations and the patient’s needs and goals. Migraine pharmacologic treatment may be acute (abortive) or preventive (prophylactic), and patients often require both. New medication devices are available or in development, including an intracutaneous, microneedle system of zolmitriptan and sumatriptan, and breath-powered powder sumatriptan intranasal treatment. Lasmiditan, a 5-HT1F receptor agonist, is in development for acute treatment, as are small molecule calcitonin gene-related peptide (CGRP) receptor antagonists (Gepants) for acute and preventive treatment. Antibodies to CGRP and its receptor are being developed for migraine prevention. All 4 treatments are effective and have, as of yet, no safety concerns.

Pharmacogenomic testing can be integrated into modern mental health practices to help select psychotropic drugs for individuals who have failed first-line evidence-based treatments. This can be done by the process of “equipoise”—namely, balancing the weight of all available evidence. That evidence now includes not only diagnosis-specific treatment guidelines and “personalized” patient information, such as an individual’s specific symptom profile, past response to medications, side effects, family history, and patient preference, but also “precision medicine,” which incorporates the ever-expanding base of pharmacogenomic evidence for how an individual’s own biomarkers alter the odds for that individual’s treatment response or treatment intolerance.

Since hearing loss is strongly linked to cognitive decline, treating hearing impairment may have the potential to prevent the onset or slow the progress of dementia.

There has been increasing recognition that antipsychotic nonadherence is common across all stages of schizophrenia, starting from the first episode. Moreover, numerous meta-analyses of the existing literature indicate superiority of long-acting injectable (LAI) over oral antipsychotics when one adjusts for the greater illness severity and duration among patients in LAI antipsychotic trials. The increasing availability of LAI antipsychotic options has raised interest in converting patients from oral medication; however, the successful transition from oral to the comparable LAI antipsychotic requires an understanding of the current extent of antipsychotic exposure, the kinetics of the LAI preparation, and the expected plasma levels achieved by the LAI formulation. The purpose of this article is to provide, in a concise format, the essential information for converting patients to the LAI forms of haloperidol, fluphenazine, risperidone, paliperidone, olanzapine, and aripiprazole from the comparable oral medication, and how the use of plasma antipsychotic levels can be invaluable for this process.

Earlier findings suggest that forensic schizophrenia patients are treated with higher doses of antipsychotics. This practice-based specificity is insufficiently studied, and clinicians’ motives regarding this practice remain poorly understood. In this editorial, the authors provide their data on treatment of forensic schizophrenia patients and identify characteristics of psychopathology and previous types of behaviors, including suicidal attempts, as potential reasons for the practice. They also emphasize that “these previous acts” often took place years ago, and suggest that current or recent aggression is unlikely the main reason for dosing, but rather the clinicians’ intention to maintain “must remain unaggressive” condition. Therefore, the authors suggest new ideas that may contribute to a better understanding of the specific prescribing patterns in the forensic population and hope that these ideas would be implemented in further well-designed prospective studies.

Alzheimer’s disease (AD) has long been recognized as a heterogeneous illness, with a common clinical presentation of progressive amnesia and less common “atypical” clinical presentations, including syndromes dominated by visual, aphasic, “frontal,” or apraxic symptoms. Our knowledge of atypical clinical phenotypes of AD comes from clinicopathologic studies, but with the growing use of in vivo molecular biomarkers of amyloid and tau pathology, we are beginning to recognize that these syndromes may not be as rare as once thought. When a clinician is evaluating a patient whose clinical phenotype is dominated by progressive aphasia, complex visual impairment, or other neuropsychiatric symptoms with relative sparing of memory, the differential diagnosis may be broader and a confident diagnosis of an atypical form of AD may require the use of molecular biomarkers. Despite the evolving sophistication in our diagnostic tools, and the acknowledgment of atypical AD syndromes in the 2011 revised diagnostic criteria for AD, the assessment of such patients still poses substantial challenges. We use a case-based approach to review the clinical and imaging phenotypes of a series of patients with typical and atypical AD, and discuss our current approach to their evaluation. One day, we hope that regardless of whether a patient exhibits typical or atypical symptoms of AD pathology, we will be able to identify the condition at a prodromal phase and institute a combination of symptomatic and disease-modifying therapies to support cognitive processes, function, and behavior, and slow or halt progression to dementia.

Research on deep brain stimulation (DBS) for treatment-resistant psychiatric disorders has established preliminary efficacy signals for treatment-resistant depression. There are only few studies on DBS that included patients suffering from bipolar disorder. This article gives an overview of these studies concerning DBS targets, antidepressant efficacy, and the occurrence of manic/hypomanic symptoms under stimulation. First, promising results show that all patients experienced significant improvement in depressive symptomatology. In a single case, hypomanic symptoms occurred, but they could be resolved by adjusting stimulation parameters. Furthermore, this article highlights important clinical differences between unipolar and bipolar depression that have to be considered throughout the course of treatment.

This article re-examines the popular concept of Internet addiction, discusses the key problems associated with it, and proposes possible alternatives. The concept of Internet addiction is inadequate for several reasons. Addiction may be a correct designation only for the minority of individuals who meet the general criteria for addiction, and it needs to be better demarcated from various patterns of excessive or abnormal use. Addiction to the Internet as a medium does not exist, although the Internet as a medium may play an important role in making some behaviors addictive. The Internet can no longer be separated from other potentially overused media, such as text messaging and gaming platforms. Internet addiction is conceptually too heterogeneous because it pertains to a variety of very different behaviors. Internet addiction should be replaced by terms that refer to the specific behaviors (eg, gaming, gambling, or sexual activity), regardless of whether these are performed online or offline.