A ttention-deficit/hyperactivity disorder (ADHD) is common, with an estimated worldwide prevalence of 5.29% among children and adolescents and 2.5% among adults. 1 DSM-5-TR classifies ADHD as a neurodevelop mental disorder, "a group of conditions with onset in the developmental period [that] typically manifest early in development, often before the child enters school." 2 Because of the expectation that ADHD symptoms emerge early in development, the diagnostic criteria specify that symptoms must have been present prior to age 12 to qualify as ADHD. However, recent years have shown a significant increase in the number of patients being diagnosed with ADHD for the first time in adulthood. One study found that the diagnosis of ADHD among adults in the United States doubled between 2007 and 2016. 3 First-line treatment for ADHD is the stimulants methylphenidate and amphetamine/dextroamphetamine. In the United States, these medications are classified as Schedule II controlled substances, indicating a high risk for abuse. However, just as ADHD diagnoses among adults have increased, so have prescriptions for stimulants. For example, Olfson et al 4 found that stimulant prescriptions among young adults increased by a factor of 10 between 1994 and 2009. The increased prevalence of adult patients diagnosed with ADHD and taking stimulants frequently places clinicians in a position to consider the validity of existing diagnoses and evaluate new patients with ADHD-related concerns. In this These steps can help ensure accurate diagnosis and optimal outcomes

F or many years, attention-deficit/hyperactivity disorder (ADHD) was thought of as a disorder of childhood; however, it is now increasingly being recognized as a chronic, lifelong disorder that persists into adulthood in approximately two-thirds of patients. 1 While our knowledge about ADHD in adults has increased, most research in this population focused on young or middle-aged adults; less is known about ADHD in older adults. Older adults with ADHD may be newly diagnosed at any point in their lives, or not at all. 2 Because ADHD may present differently in older adults than in children or young adults, and because it may impair domains of life in different ways, a closer look at late-life ADHD is needed. This article summarizes the literature on the prevalence, impairment, diagnosis, and treatment of ADHD in adults age >60. Few studies have examined the age-specific prevalence of ADHD among older adults. 3 Compared with childhood ADHD, adult ADHD is relatively neglected in epidemiological studies, largely due to the absence of well-established, validated diagnostic criteria. 1,4 Some experts have noted that DSM-5's ADHD criteria were designed for diagnosing children, and the children-focused symptom threshold may not be useful for adults because ADHD symptoms decline substantially with age. 2 One study evaluating DSM-5 ADHD criteria in young adults (N = 4,000, age 18 to 19) found ADHD was better diagnosed when the required number of clinically relevant inattention and hyperactivity symptoms was reduced from 6 to 5 for each category. 5 They also found the DSM-5 age-at-onset criterion of symptoms present

Ms. A, age 20, presents to the clinic after experiencing difficulty sleeping, depressed mood, fatigue, and difficulty concentrating.Her psychiatric history includes bipolar II disorder (BD II), predominantly with depressive episodes.Ms. A's current medications include a combination of lamotrigine 200 mg/d and bupropion extended-release 450 mg/d, and her symptoms were well maintained until 2 weeks ago.When her psychiatrist performs a medication reconciliation at her medication management appointment, Ms.A indicates she started taking an oral contraceptive, ethinyl estradiol and norgestimate, approximately 1 month ago for management of endometriosis symptoms.She is not currently taking any other medications or supplements.Lamotrigine is indicated for epilepsy and as maintenance treatment for BD I.It is also used off-label to treat other mood disorders.After oral administration, lamotrigine is rapidly and fully absorbed with a high bioavailability (98%).The principal metabolic pathway is via glucuronic acid conjugation, leading to the major inactive metabolite 2-N-glucuronide.Minor metabolites include 5-N-glucuronide and a 2-N-glucuronide metabolite. 1 Combined oral contraceptives contain an estrogen component, typically ethinyl estradiol, and a progestin component, which varies based on the specific formulation.The metabolism of ethinyl estradiol occurs through cytochrome P450 (CYP)3A4, CYP2C9, sulfation, and glucuronidation.For progestin-the second component of combined oral contraceptives and the lone com ponent of progestin-only oral contraceptives-metabolism occurs via CYP3A4 and conjugation reactions. 2This article focuses on lamotrigine interactions specifically with oral contraceptives, but it is important to note that other formulations of combined hormonal contraceptives, such as the combined contraceptive patch Lamotrigine interactions with oral contraceptives

As an emergency department (ED) psychiatrist with 25 years of experience working in a large city, I am growing increasingly concerned about the escalating number of individuals experiencing homelessness in urban areas.

hile most psychiatric treatments have traditionally consisted of pharmacotherapy with oral medications, a better understanding of the pathophysiology underlying many mental illnesses has led to the recent increased use of treatments that require specialized administration and the creation of a subspecialty called interventional psychiatry. In Part 1 of this 2-part article ("Interventional psychiatry [

Deaths of children who are killed by their parents often make the news.Cases of maternal infanticide may be particularly shocking, since women are expected to be selfless nurturers.Yet when a child is murdered, the most common perpetrator is their parent, and mothers and fathers kill at similar rates. 1 As psychiatrists, we may see these cases in the news and worry about the risks of our own patients killing their children.In approximately 500 cases annually, an American parent is arrested for the homicide of their child. 2This is not even the entire story, since a large percentage of such cases end in suicide-and no arrest.This article reviews the reasons parents kill their children, and considers common characteristics of these parents, dispelling some myths, before discussing the importance of prevention efforts. Types of child murder by parentsChild murder by parents is termed filicide.Infanticide has various meanings but often refers to the murder of a child younger than age 1.Approximately 2 dozen nations (but not the United States) have Infanticide Acts that decrease the penalty for mothers who kill their young child. 3eonaticide refers to murder of the infant at birth or in the first day of life. 4 Awareness of the characteristics and motives can help target prevention effortsChild murder by parents: Toward prevention CHRISTINAROSEPIX/

Ms. V, age 58, presents to the emergency department after falling in the middle of the night while walking to the bathroom.Her medical history includes bipolar I disorder (BDI).According to her granddaughter, Ms. V has been stable on lithium 600 mg twice daily for 1 to 2 years.Her laboratory workup shows a serum creatinine level of 0.93 mg/dL (reference range 0.6 to 1.2 mg/dL), high sodium (154 mEq/L; reference range 135 to 145 mEq/L), and a lithium level of 0.9 mEq/L (therapeutic range 0.6 to 1.2 mEq/L).On Day 2 of admission, Ms. V's sodium level remains high (152 mEq/L), her urine output is 5 L/d (normal output <2 L/d), and her serum osmolality is high (326 mmol/kg; reference range 275 to 295 mmol/kg).After additional questioning, Ms. V says for the past 3 weeks she has been urinating approximately 4 times per night and experiencing excessive thirst.Given her laboratory values and physical presentation, a desmopressin challenge test is performed and confirms a diagnosis of lithium-induced nephrogenic diabetes insipidus (Li-NDI).Nephrogenic diabetes insipidus (NDI) occurs when the kidneys become unresponsive to the action of antidiuretic hormone (ADH; also known as vasopressin). 1The most common cause of NDI is lithium.The prevalence varies from 50% to 73% with long-term lithium use. 1,2It is important to recognize the homeostatic regulation of water prior to understanding Li-NDI.The excretion of water is regulated by ADH.ADH binds to the vasopressin receptors on the basolateral membrane of the collecting duct cells.This stimulates Gs protein and adenylate cyclase, which subsequently increase intracellular cyclic adenosine monophosphate (cAMP). 1 Eventually, this leads to the activation of protein kinase A and phosphorylation of aquaporin 2 (AQP2) water channels.The AQP2 channels redistribute from storage vesicles to the apical membrane and the membrane becomes permeable to water, allowing for reabsorption. 1,

Readers' Forum nationwide shortage."Even with the most difficult insurers, the response has been "a temporary 3-month authorization has been granted," which is at least a small victory for our desperate patients and busy prescribers who are both struggling to negotiate a fragmented health care system.

Answer the challenge questions at MDedge.com/ psychiatry and see how your colleagues responded