CGPR: What is your clinical background, and how does it shape your approach to ADHD in older adults?
Dr. Anbarasan: I’m double board-certified in neurology and psychiatry, and my clinical work sits at that intersection. I primarily treat outpatients with neuropsychiatric conditions, including adult ADHD. That dual training naturally pushes me to think broadly when older adults present with attention or executive concerns: Is this lifelong ADHD? A mood or sleep issue? Medication effects? Or early neurocognitive disorder? Because the differential is wider and medical comorbidity is more common in later life, I place a strong emphasis on diagnostic clarity.

CGPR: How do you approach diagnosing ADHD in older adults and distinguishing it from other causes of cognitive symptoms?
Dr. Anbarasan: I start with a careful longitudinal assessment. ADHD is a neurodevelopmental disorder, so symptoms should trace back to childhood, even if the person was never diagnosed or relied on compensatory strategies for years. When collateral is available, I include input from family members or long-term partners. In many older adults, collateral is limited, so I rely on a detailed patient history to identify lifelong patterns of inattention, disorganization, impulsivity, and functional impairment across settings. The key distinction from neurocognitive disorders is trajectory: ADHD reflects stable executive difficulties, while dementia involves a decline from prior functioning, often affecting memory consolidation, language, or visuospatial skills. When the picture is unclear, longitudinal follow-up can be very helpful and prevents premature medication exposure. I also consider common mimics such as obstructive sleep apnea, depression, anxiety, medication effects, and metabolic or endocrine conditions. Given the frequency of comorbidity and polypharmacy in late life, I review sleep, substance use, and the full medication list, including over-the-counter agents and supplements. Only after excluding reversible or progressive contributors do I move toward medications.

CGPR: Let’s talk about baseline steps before initiating a stimulant.
Dr. Anbarasan: Before prescribing, I clarify treatment goals. Are we trying to improve bill payment, appointment adherence, caregiving responsibilities, or workplace productivity? We shouldn’t start a stimulant without defined functional targets. I screen for comorbid mood disorders, anxiety, bipolar disorder, and substance use, as these influence medication choice and risk. I always collect baseline vital signs (heart rate, blood pressure, and weight). I also document baseline sleep and appetite, because these are commonly affected by stimulants and will need monitoring. Finally, I emphasize that medication is not a magic bullet. I speak about the importance of behavioral supports like structured routines, digital reminders, and environmental organization. The medication may make it easier to implement those strategies, but it does not replace them.

CGPR: How do you approach cardiovascular risk assessment in older adults?
Dr. Anbarasan: In assessing cardiovascular risk, I evaluate for uncontrolled hypertension, symptomatic arrhythmias, prior ischemic heart disease, exertional chest pain, and a strong family history of sudden cardiac death. When these issues are present, I collaborate with the patient’s cardiologist or primary care clinician before starting stimulants and may defer treatment or consider a non-stimulant based on that input. Cumulative ADHD medication use has been linked to a modest increase in cardiovascular risk, particularly hypertension and arterial disease (Zhang L et al, JAMA Psychiatry 2024;81(2):178–187). I document baseline blood pressure and heart rate, repeat these within a month of stimulant initiation, and monitor at least every six months thereafter, with closer follow-up for patients with cardiac comorbidity or after dose change. Although not required by guidelines, I often obtain a baseline ECG as a useful reference if concerns emerge later. The goal is not to avoid stimulants reflexively, but to understand baseline risk and monitor thoughtfully.

“The key question is stability: If cardiac disease is active or unstable, I hold off on stimulants and atomoxetine; if it’s well managed, a cautious low-dose trial with monitoring may be appropriate.”

Deepti Anbarasan, MD 

CGPR: When would you avoid prescribing a stimulant?
Dr. Anbarasan: There are few absolute contraindications, but poorly controlled cardiovascular disease gives me pause. Older adults already carry higher baseline cardiovascular risk, and one study found about a 40% increased risk in cardiovascular events during the first 30 days after starting a stimulant in this age group (Tadrous M et al, JAMA Netw Open 2021;4(10):e2130795). In practice, if a patient has uncontrolled hypertension or symptomatic arrhythmias, I wait until things are stabilized. A history of paroxysmal atrial fibrillation isn’t a dealbreaker, but I want to see that the rate and rhythm are well controlled and will often loop in cardiology. In higher-risk situations, alpha-2 agonists may be reasonable alternatives, though they’re not risk-free and may interact with other cardiac medications, so coordination still matters. The key question is stability: If cardiac disease is active or unstable, I hold off on stimulants and atomoxetine; if it’s well managed, a cautious low-dose trial with monitoring may be appropriate. I am also cautious in patients with a history of psychosis or mania, since stimulants can worsen psychotic symptoms or trigger manic episodes.

CGPR: How does dosing differ in older adults compared to younger patients?
Dr. Anbarasan: Guidance specific to older adults is limited (Dobrosavljevic M et al, Expert Rev Neurother 2023;23(10):883–893). FDA labeling addresses adults up to age 65, and formal US dosing guidelines for adult ADHD are lacking, though stimulants remain first line by expert consensus. I follow a “start low and go slow” approach, beginning at one-quarter to one-half the usual adult dose and waiting at least two weeks before adjusting. Age-related changes in metabolism and body composition can increase medication exposure, making older adults more sensitive to both benefits and side effects. I monitor closely for sleep disturbance and appetite suppression, which may be particularly problematic in older adults (Torgersen T et al, Neuropsychiatr Dis Treat 2016;12:79–87). These effects can contribute to weight loss, frailty, cognitive or mood changes, and fall risk. Titrate deliberately. I generally favor methylphenidate over amphetamine formulations due to a more tolerable side effect profile and broader evidence in geriatric populations, including depression and apathy. I might start methylphenidate IR at 2.5 mg each morning and increase by 2.5 mg after 2–3 weeks, either by increasing the morning dose or adding a midday dose.

From the Expert Q&A
“Tailoring ADHD Medication for Older Patients”
by Deepti Anbarasan, MD
The Carlat Geriatric Psychiatry Report, Volume 5, Issue 3 & 4
April/May/June 2026
www.thecarlatreport.com

CGPR: Do you favor short-acting or long-acting stimulants in older adults?
Dr. Anbarasan: Although most adult ADHD trials focus on extended-release formulations, I often begin with short-acting stimulants in older adults. These allow closer monitoring of tolerability and duration of effect and are easier to adjust if appetite suppression or insomnia emerges. This approach mirrors pediatric practice: Establish tolerability first, then transition to long-acting if appropriate. Once the patient responds well and tolerates the medication, extended-release formulations may improve convenience and adherence. In patients with a history of medication misuse, I am more likely to start with an extended-release formulation, such as OROS methylphenidate (Concerta), which has abuse deterrent properties due to its osmotic release design. In this group, I use caution with immediate-release tablets.

CGPR: When are non-stimulants particularly appropriate?
Dr. Anbarasan: I tend to reach for non-stimulants when there’s a history of substance use, severe anxiety, bipolar disorder, or significant insomnia. They can be helpful alternatives, but they’re not risk-free. Atomoxetine and viloxazine can increase heart rate and blood pressure, so they don’t offer a clear cardiovascular advantage. Atomoxetine also carries a risk of severe hepatotoxicity, so patients should report symptoms like jaundice, dark urine, or right upper quadrant pain. If cardiovascular disease is unstable or poorly controlled, I defer pharmacologic treatment altogether and coordinate care before starting any ADHD medication. I generally avoid alpha-2 agonists like clonidine and guanfacine in older adults due to orthostasis, bradycardia, sedation, and fall risk. One practical pearl: Viloxazine capsules can be opened and sprinkled on food, while atomoxetine must be swallowed whole, which may make viloxazine a better option for patients with dysphagia or feeding tubes.

CGPR: How do age-related pharmacologic changes influence prescribing?
Dr. Anbarasan: Aging affects both pharmacokinetics and pharmacodynamics in ways that matter clinically. Hepatic and renal clearance decline, and body composition shifts toward more fat and less water. Clinically, that means medications may feel stronger, last longer, and accumulate more easily. Older adults are also more sensitive to side effects like insomnia, appetite loss, anxiety, blood pressure changes, and dizziness. For stimulants, cardiovascular effects are the main concern. Initiation in older adults is linked to an increased risk of cardiovascular events, particularly in the first 30 days, with risk attenuating over time (Tadrous et al, 2021). I start low and titrate slowly, since doses that work in younger adults can be excessive in this population. With non-stimulants, the metabolic pathways don’t change with age, but drug exposure can still increase due to reduced clearance. Polypharmacy is the bigger issue. Atomoxetine (CYP2D6) can reach markedly higher levels (up to 10-fold) with inhibitors like paroxetine or fluoxetine, or in poor metabolizers. These aren’t age-specific mechanisms, but they matter more in older adults because of medication burden and reduced physiologic reserve.

CGPR: What medication interactions should clinicians consider?
Dr. Anbarasan: Polypharmacy is the norm in older adults, so I start with a thorough medication review. Stimulants have relatively few direct drug-drug interactions, but additive effects matter. Combining stimulants with SNRIs or bupropion can increase blood pressure and heart rate due to overlapping sympathomimetic effects. One nuance that’s easy to miss: Amphetamines are partly metabolized by CYP2D6. This doesn’t always appear in interaction checkers, but FDA labeling recommends lower starting doses and closer monitoring with strong CYP2D6 inhibitors. Bupropion is a potent CYP2D6 inhibitor (especially at or over 300 mg), so I’m cautious with this combination, as it may increase stimulant exposure beyond additive noradrenergic effects. In patients with hypertension, I recommend weekly home vitals during titration, then every 3–6 months once stable, with individualized targets (often <130–135/80–85). I also review over-the-counter agents. Decongestants like pseudoephedrine or phenylephrine can amplify sympathomimetic effects. The patient’s full medication list often determines whether a stimulant or non-stimulant makes the most sense.

CGPR: Are there non-cardiovascular comorbidities to consider?
Dr. Anbarasan: Yes. Sleep disorders, anxiety, and substance use are the ones I think about most often. If an older adult already has chronic insomnia or fragmented sleep, I’m more cautious with stimulants. I may favor shorter-acting formulations (eg, Ritalin IR, Adderall IR) and keep doses low. In patients with comorbid anxiety, stimulants can feel activating or jittery, so I might lean toward atomoxetine or viloxazine. Viloxazine is particularly interesting because, in addition to norepinephrine modulation, it has downstream serotonergic activity that may offer some benefit for anxiety. For individuals with significant substance use disorders, I generally favor non-stimulants, not only because of misuse potential but also due to safety considerations when substances are being used concurrently. There is also emerging, though controversial, evidence linking ADHD with increased risk of later-life neurocognitive disorders (Levine SZ et al, JAMA Netw Open 2023;6(10):e2338088). In mild cognitive impairment, stimulants may briefly improve apathy, although evidence in moderate to severe dementia is limited (Mintzer J et al, JAMA Neurol 2021;78(11):1324–1332). In select cases with severe apathy, a cautious trial may still be reasonable.

CGPR: How should patients be monitored after starting treatment?
Dr. Anbarasan: At follow-up visits, I reassess functional targets. Are appointments being kept, bills paid on time, and social obligations met? I also review adherence, barriers to use, and changes in sleep and appetite, while monitoring weight, blood pressure, and heart rate. For alpha-2 agonists, I ask specifically about dizziness, lightheadedness, and daytime sedation. I reconsider the treatment strategy if resting heart rate drops below 55 bpm, systolic blood pressure drops more than about 15–20 mmHg from baseline, or the patient reports orthostatic symptoms. Ongoing shared goal setting matters here, with adjustments to dose or timing based on both benefit and tolerability. I also emphasize that medication works best alongside practical behavioral strategies that reduce executive burden—using a single calendar, setting alarms or written reminders, and simplifying routines so tasks occur at consistent times. Reducing multitasking and finding ways to automate tasks, such as using pillboxes or autopay for bills, can make daily life smoother. Many older patients find these strategies easier to adopt once medication has helped improve attention and organization.

CGPR: Thank you for your time, Dr. Anbarasan.