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Medscape
4 hours ago
- Health
- Medscape
Uncontrolled Movements, Anger, and Insomnia
Editor's Note: The Case Challenge series includes difficult-to-diagnose conditions, some of which are not frequently encountered by most clinicians, but are nonetheless important to accurately recognize. Test your diagnostic and treatment skills using the following patient scenario and corresponding questions. If you have a case that you would like to suggest for a future Case Challenge, please email us at ccsuggestions@ with the subject line "Case Challenge Suggestion." We look forward to hearing from you. Background A 35-year-old man presents to the neurology clinic due to abnormal movements over the past 6 years. The involuntary movements began in the right upper limb, followed sequentially by the left upper limb, left lower limb, and finally the head and neck. The movements occur during wakefulness and are absent in sleep. They are described as jerky and nonpurposeful. His gait has assumed a dancelike character. He also has had behavioral changes that include frequent outbursts of anger, aggressive behavior, depressive mood, and insomnia. His abnormal movements are aggravated during outbursts of anger and disturbances in mood. He has no weakness in any limbs but is unable to perform regular household activities. Family members have also noted memory impairment. He has been unable to continue his work as a machine operator for the past 3 months. He has no history of psychoactive drug intake, including phenytoin, phenothiazines, haloperidol, L-dopa, lithium, isoniazid, amphetamines, tricyclic antidepressants, or any other relevant drugs. He reports no history of chest pain, breathlessness, or joint pain. His family history includes a paternal grandfather and father who had similar forms of abnormal movements and died at the age of 60 years and 55 years, respectively. The patient has five siblings (two brothers, three sisters). His elder brother died by suicide at age 25 years, and his elder sister died at age 33 years. Both had abnormal movements and abnormal behaviors. One of his younger sisters (age 22 years) also has similar abnormal movements and depressed attitude. His younger brother (age 17 years) and other younger sister (age 14 years) are healthy and symptom-free. The patient's children, an 8-year-old son and a 10-year-old daughter, are symptom-free. His past medical history is positive for hypertension, which is well controlled with lisinopril (20 mg daily). He has no surgical history. He does not smoke, drink, or use recreational drugs. Physical Examination and Workup A general examination reveals a pleasant man who is well built and in no acute distress. His blood pressure is 140/80 mm Hg, his heart rate is 78 beats/min, his respiratory rate is 12 breaths/min, his SpO 2 level is 98% on room air, and his body mass index (BMI) is 20. He is afebrile. A cardiovascular examination reveals normal peripheral pulses and normal heart findings. A chest examination reveals normal auscultation and expansion. His abdomen is soft. Head, eyes, ears, nose, and throat (HEENT) examination findings are unremarkable. He does not have a skin rash. A visual examination reveals normal acuity, field, and fundi. His affect is flat. A neurologic examination of the higher mental functions reveals that the patient is awake and alert, with normal orientation, attention, concentration, fund of knowledge, and language function. His memory is impaired, with recall one-third at 3 minutes. He has a normal past memory. His speech is normal. A cranial nerve examination reveals normal extraocular movements, increased blink rate, normal facial sensation, a symmetric face with abnormal fidgety movement, normal hearing, and normal palate movement. He has abnormal tongue movement and cannot protrude his tongue more than 20 seconds (darting tongue movement). He has normal shoulder shrug. No Kayser-Fleischer ring is noted during slit-lamp examination. An examination of the motor system reveals decreased muscle tone, normal bulk, and 5/5 strength in both upper and lower extremities. No atrophy or fasciculation is noted. Deep tendon reflexes are normal (2+ with flexor planters). Sensory examination findings are normal. Finger-nose test findings are normal. An examination of the extrapyramidal system reveals reduced tone and involuntary choreoathetoid movements that affect both upper and lower extremities as well as his face. He has a dancing gait. Diagnostic tests reveal normal complete blood cell count (CBC) and comprehensive metabolic panel findings. He has normal serum findings and urine copper levels. His erythrocyte sedimentation rate (ESR) is 22 mm/hr (reference range, 0-22 mm/hr). He has normal ECG findings, a normal thyroid-stimulating hormone (TSH) level, a normal transthoracic echo (with ejection fraction 65%), and normal chest radiography findings. Brain MRI can be used to evaluate for selective atrophy of deep gray structures, to document disease burden, and to provide a baseline for future comparison. Whole-body 18-FDG PET/CT may be used to screen for occult neoplasm and paraneoplastic chorea, but this is exceedingly rare and typically subacute. NMDA receptor antibody panel may be used to investigate for autoimmune encephalitic chorea, but the features of this (ie, seizures, psychosis, and autonomic instability) are absent in this case. RPR and FTA-ABS may be used to evaluate for neurosyphilitic chorea, but this is also very uncommon and unnecessary without risk factors or acute symptoms. In this patient, brain MRI reveals evidence of bilateral caudate atrophy, with increased intercaudate distance (Figure). Figure. Cerebrospinal fluid (CSF) examination findings are normal. Discussion This 35-year-old man has Huntington disease. He has insidious-onset, slowly progressive movement disorder, and movements are absent during sleep. His movements are described as choreoathetoid. He has family history that suggests autosomal dominant transmission. Apart from the movement disorder, he also has neuropsychiatric manifestations, with death at an early age in the family. A CT scan of the head revealed evidence of caudate nucleus atrophy. Brain MRI revealed evidence of caudate atrophy (Figure). Figure. In evaluating the differential diagnoses, the patient has no history of antipsychotic medication use to suggest tardive dyskinesia. He has no clinical or diagnostic evidence of infection or heart involvement, which makes Sydenham chorea unlikely. No acanthocytes were observed, helping to exclude neuroacanthocytosis. The strong family history of progressive abnormal movements and neuropsychiatric symptoms across generations supports a genetic etiology, specifically autosomal-dominant Huntington disease. Huntington disease is a rare neurodegenerative disorder of the central nervous system (CNS) characterized by choreiform movements, behavioral and psychiatric disturbances, and dementia.[1] Huntington disease is caused by an autosomal-dominantly inherited expansion of CAG trinucleotide repeats in the huntingtin ( HTT ) gene on chromosome 4; this leads to production of a mutant huntingtin (mHTT) protein, with an abnormally long polyglutamine repeat.[2] Individuals with more than 39 CAG repeats develop the disease, whereas reduced penetrance is seen in those with 36-39 CAG repeats. The disease can be anticipated when the gene is passed down the paternal line, as in this case; a father with a CAG repeat length in the intermediate range may have a child with an expanded pathogenic repeat length. This is because sperm from males shows greater repeat variability and larger repeat sizes than somatic tissues. Mutant huntingtin protein leads to death and neuronal dysfunction through various mechanisms. Postmortem studies reveal diffuse atrophy of the caudate and putamen. The progressive worsening of Huntington disease leads to a bedridden state with cognitive deterioration, and death typically occurs about 20 years after the onset of symptoms.[3] Prevalence in the white population is estimated at 1 in 10,000 to 1 in 20,000. The mean age at symptom onset is 30-50 years. In some cases, symptoms begin before age 20 years, with behavior disturbances and learning difficulties at school; this is termed juvenile Huntington disease (Westphal disease).[4] The first description, by Waters, dates to 1842. However, after a description in 1872 by George Huntington, it became known as Huntington chorea. In 1983, a linkage on chromosome 4 was established, and in 1993 the gene for Huntington disease was found.[1] Diagnosis of Huntington disease is confirmed by demonstration of autosomal dominant transmission or gene testing in the presence of clinical features.[5] The clinical features of Huntington disease consist of motor, cognitive, and neuropsychiatric manifestations. Huntington disease has a biphasic course of hyperkinetic phase with chorea in the early stages of disease that then plateaus into a hypokinetic phase, consisting of bradykinesia dystonia, balance issues, and gait disturbance. The younger-onset variant is associated with predominant bradykinesia.[6] Cognitive disturbance can be seen many years before other symptom onset and is characterized by impaired emotion recognition, processing speed, and executive function abnormality. Neuropsychiatric symptoms widely vary, including apathy, anxiety, irritability, depression, obsessive-compulsive behavior, and psychosis. A lack of awareness of early and progressing behavioral, cognitive, and motor symptoms is a hallmark of Huntington disease. This unawareness is caused by the disease itself (specifically, impaired insight or anosognosia) and is not the result of intentional denial, avoidance, or suppression of symptoms.[7] Therefore, a comprehensive history, including information from a knowledgeable family member/caregiver, is advisable.[7] Numerous conditions can mimic Huntington disease, including a spinal cerebellar ataxia 17, spinocerebellar ataxia 1-3, and Friedreich ataxia, which involve neuropathy. If seizures are also present, dentatorubropallidoluysian atrophy should be considered. Acanthocytes are seen in patients with neuroacanthocytosis.[8-10] Isolated chorea can be seen in acquired conditions, including chorea gravidarum, systemic lupus erythematosus, antiphospholipid syndrome, thyrotoxicosis, postinfectious syndromes, polycythemia vera, and some drug use. Genetic testing for the mHTT mutation can be either diagnostic or predictive.[6] A diagnostic test may be performed when a patient presents with typical motor features of Huntington disease. Prior to testing, the patient should be informed about Huntington disease and its hereditary nature, as a positive test result has implications for the patient and family. Predictive testing is performed in asymptomatic patients, mostly for reproductive reasons. Treatment of Huntington Disease The optimal management of Huntington disease involves a multidisciplinary approach that includes neurology, nurses, physical therapy, speech-language pathology, and dietitians and other healthcare professionals. The goal is to optimize the quality of life based on the changing need of the patient. These consist of combined pharmacologic and lifestyle changes, including behavioral therapy. Symptoms may be worsened by stress, fatigue, and intercurrent disorders (eg, anxiety, digestive disorders, infectious or painful conditions), so these aspects must be assessed and treated alongside the primary symptoms of Huntington disease.[3] In clinical practice, information about symptoms should be obtained from both the patient and caregivers, since patients may have impaired awareness of their condition.[11] Identifying coexisting psychiatric symptoms, comorbid medical conditions, and environmental factors is crucial.[11] Educating caregivers about the nature and presentation of symptoms and methods to modify triggers is also vital.[11] Medication choices should be guided by coexisting symptoms and disease stage, and regular reassessment of drug need and potential for dose reduction is important because of adverse effects that can mimic disease progression.[11] Nonpharmacologic interventions, including behavioral therapies and environmental modifications, should be prioritized for neuropsychiatric symptoms in Huntington disease. Pharmacologic agents may be considered if these measures are insufficient, and consultation with a psychiatrist knowledgeable in Huntington disease is recommended for individuals whose symptoms are resistant to standard pharmacologic therapy.[11] Tetrabenazine and its modified version, deutetrabenazine, are commonly used to treat choreiform movements. Side effects of tetrabenazine can include depression, anxiety, sedation, sleep problems, restlessness, and parkinsonism.[7] Citalopram is a selective serotonin reuptake inhibitor used to manage depression. Modafinil and atomoxetine are used to manage apathy. Tiapride, although unavailable in the United States, is considered a first-line treatment option for chorea outside the United States.[7] Other antipsychotics such as olanzapine, risperidone, and quetiapine are also used to manage chorea. Risperidone may also help with psychomotor restlessness, and olanzapine and quetiapine can have additional benefits like weight gain (which can be desirable in Huntington disease) and mood stabilization. Haloperidol has also shown effectiveness.[7] Medications used to suppress chorea (eg, tetrabenazine and deutetrabenazine and certain antipsychotics) should be used sparingly and mainly for subjectively disabling hyperkinesias, starting at low doses and titrating gradually. They make take 4-6 weeks to show results.[7] The choice of medication depends on the individual patient's symptoms, tolerability, and co-existing conditions.[7] Evidence regarding the treatment of psychiatric symptoms in Huntington disease is limited, with recommendations often based on expert opinion owing to a lack of robust controlled studies.[7,11] Nonpharmacologic interventions such as cognitive-behavioral therapy and psychodynamic therapy are recommended, especially for depression, anxiety, obsessive-compulsive behaviors, and irritability. Behavioral strategies (eg, structured routines and distraction) are important for managing irritability and agitation.[3,11] Depression: Selective serotonin reuptake inhibitors (SSRIs) such as citalopram, fluoxetine, paroxetine, sertraline, and venlafaxine are recommended as pharmacologic options. [3,7] Mianserin (unavailable in the United States) or mirtazapine are alternatives, particularly in patients with sleep disruption. [3,7,11] Electroconvulsive therapy (ECT) may be considered for severe or resistant cases, although it can significantly impair short-term memory. [3,7] Mianserin (unavailable in the United States) or mirtazapine are alternatives, particularly in patients with sleep disruption. Electroconvulsive therapy (ECT) may be considered for severe or resistant cases, although it can significantly impair short-term memory. Anxiety: SSRIs or serotonin-noradrenaline reuptake inhibitors (SNRIs) are first-line treatments, especially when anxiety coexists with depression. [3,11] Mirtazapine is an option in patients with sleep disorders. [11] Long-term use of benzodiazepines is generally discouraged for ambulatory individuals because of the risk of falls and dependence but can be used short-term or as needed. [3,11] Mirtazapine is an option in patients with sleep disorders. Long-term use of benzodiazepines is generally discouraged for ambulatory individuals because of the risk of falls and dependence but can be used short-term or as needed. Obsessive-compulsive behaviors/perseverations: For true obsessive-compulsive phenomena, SSRIs are considered first-line treatment. [3] Olanzapine and risperidone may also be valuable for ideational perseverations, particularly if associated with irritability. [3] Clomipramine is an option, especially if needed for coexisting obsessive perseverative behaviors. [11] Olanzapine and risperidone may also be valuable for ideational perseverations, particularly if associated with irritability. Clomipramine is an option, especially if needed for coexisting obsessive perseverative behaviors. Irritability and aggression: SSRIs are a first-line treatment. [3] For aggressive behavior, neuroleptics are recommended. [3,7] Mood stabilizers (eg, valproate, lamotrigine, lithium, carbamazepine) can be added if irritability is resistant to other treatments or for mood lability. Risperidone and olanzapine may help reduce irritability. [3,7] For aggressive behavior, neuroleptics are recommended. Mood stabilizers (eg, valproate, lamotrigine, lithium, carbamazepine) can be added if irritability is resistant to other treatments or for mood lability. Risperidone and olanzapine may help reduce irritability. Psychosis (hallucinations/delusions): Second-generation neuroleptics (antipsychotics) are the first-line pharmacologic treatment. [3,7,11] Options include olanzapine, risperidone, quetiapine, aripiprazole, and haloperidol. [7] Clozapine may be considered for severe or resistant cases, particularly in akinetic forms of Huntington disease but requires regular monitoring. [3,7,11] Underlying causes, such as the use of psychotropic agents or somatic triggers, should be investigated and addressed. [3,11] Options include olanzapine, risperidone, quetiapine, aripiprazole, and haloperidol. Clozapine may be considered for severe or resistant cases, particularly in akinetic forms of Huntington disease but requires regular monitoring. Underlying causes, such as the use of psychotropic agents or somatic triggers, should be investigated and addressed. Apathy: Personalized cognitive stimulation and structured routines and activities are recommended.[3,7,11] If depression is suspected as a contributor, an SSRI should be tried.[3,11] In patients without depression, activating antidepressants or stimulant drugs (eg, methylphenidate, atomoxetine, modafinil) may be considered.[11] Sedative medications may increase apathy, so their dosage should be monitored or reduced.[3,11] Currently, no pharmacological treatment is specifically recommended for cognitive symptoms in Huntington disease.[3,7] Rehabilitation strategies, including speech therapy, occupational therapy, cognitive and psychomotor therapy, may help transiently improve or stabilize cognitive functions.[3,7] Coping strategies can be useful as an alternative to medication. Certain medications, such as sedative drugs, neuroleptics, and tetrabenazine, can negatively affect memory, executive functions, and attention.[3] Apart from symptomatic treatment, pharmacologic agents have failed to show benefit in clinical trials as disease-modifying agents. The most promising approaches in regard to disease modification are emerging therapies aimed at lowering levels of mHTT by targeting either the DNA or RNA of the mHTT gene.[12] RNA-targeting using antisense oligonucleotides (ASOs) have shown disappointing results in clinical trials. This has shifted significant research focus and toward orally available small molecules that modify HTT mRNA splicing, thereby reducing mHTT protein production. DNA-targeting approaches using gene editing tools like CRISPR/Cas9, while demonstrating success in preclinical models, remain in the early stages of development.[13,14] The patient in this case was diagnosed with Huntington disease with CAG repeat 78. He was started on tetrabenazine for abnormal movements and citalopram for depression. He opted to apply for federal disability. His children are asymptomatic, and the family decided not to investigate until symptoms develop or they are age 18 years.
Medscape
a day ago
- Health
- Medscape
Rapid Review: Cervical Cancer
Although often preventable, cervical cancer continues to be underdiagnosed in areas lacking access to routine Pap smears or human papillomavirus (HPV) testing. Screening, along with public health initiatives promoting HPV vaccination, are central to global elimination efforts. Advances in treatment— including minimally invasive surgery, targeted therapy, and immunotherapy — have also expanded options for individualized care. According to a recent comprehensive review and meta-analysis, AI-assisted colposcopy outperformed clinicians in all comparative measurements, including accuracy, sensitivity, specificity, positive predictive value, and negative predictive value. Specifically, AI assessment had an accuracy of 81% compared to 74% by clinicians, with the biggest difference seen in specificity where AI achieved 83% compared to 67%. AI also achieved high levels of accuracy when assessing pap smears, with an overall accuracy of 94%. Identification of these pathological changes are important; when high-risk HPV types persist, they can integrate into the host genome and trigger a series of molecular changes. These changes disrupt normal cell cycle regulation and can lead to the development of cervical intraepithelial neoplasia (CIN), which can progress from low-grade lesions to high-grade dysplasia and eventually invasive carcinoma if left untreated. Learn more about the presentation of cervical cancer. A recent cross-sectional analysis of the National Immunization Survey-Teen register found that 'safety concerns' was the most common reason for vaccine hesitancy among parents of adolescents eligible for the HPV vaccine, and that this has been an increasing trend throughout the past decade, rising from 17.5% in 2014 to 29.1% in 2020. In contrast, other reasons for vaccine hesitancy such as 'not necessary,' 'lack of knowledge,' and 'not sexually active' all saw a decreasing trend throughout this time. HPV vaccination disparities are most pronounced in adolescents from rural areas due to reduced access to healthcare and limited provider recommendation. HPV vaccination, particularly when administered before the onset of sexual activity, significantly reduces the risk of developing high-grade cervical lesions. Learn more about screening guidelines for cervical cancer. For average-risk women aged 30-65, the USPSTF recommends one of three screening strategies: cytology alone every 3 years, high-risk HPV testing alone every 5 years, or co-testing (cytology + HPV) every 5 years. Annual screening is not recommended due to lack of additional benefit and potential harms such as overtreatment. Colposcopy is a diagnostic procedure, not a screening method, and is not used routinely in women without abnormal screening results. Learn more about the workup for patients suspected of cervical cancer. Current HPV testing is more sensitive than cytology for detecting CIN, and cytology alone may miss some precancerous lesions that HPV testing would detect. In addition to greater sensitivity, HPV testing allows for longer screening intervals, which can reduce the burden of testing in patients unnecessary follow-up procedures. Learn more about approach considerations in patients with cervical cancer. The USPSTF recommends that routine cervical cancer screening be discontinued in women older than 65 years who are not at high risk and have had an adequate history of prior screening. Adequate prior screening is specifically defined as having either three consecutive negative cytology (Pap smear) results within the past 10 years or two consecutive negative high-risk human papillomavirus (hrHPV) tests within the same timeframe, with the most recent test conducted within the last 5 years. This guidance reflects the understanding that the risk of developing cervical cancer after age 65 is very low in women who have had regular negative screenings and no history of cervical precancer or cancer. However, it is important to note that women with a history of high-grade precancerous lesions (such as CIN2 or CIN3), cervical cancer, or those who have not been adequately screened should continue regular surveillance past age 65. This recommendation is part of a broader risk-based approach that aims to balance early detection with the potential harms of over-screening. Learn more about treatment options for patients once diagnosed with cervical cancer.
Medscape
a day ago
- Health
- Medscape
Prevention, Screening, Treatment: Impact on Cancer Deaths
This transcript has been edited for clarity. Hello. I'm Dr Maurie Markman from City of Hope, and I'd like to discuss a very important study. I think many of you may have heard about this, but it's important to emphasize what these investigators reported in terms of the impact of what we are doing in the cancer world today and, in my opinion, what the focus needs to be on in the future. The paper I'm referring to is "Estimation of Cancer Deaths Averted From Prevention, Screening, and Treatment Efforts, 1975-2020," published in JAMA Oncology . This was a very interesting effort; there was modeling done, and assumptions were made, in order to do what these investigators did. But this is, I think, very high-quality and reasonable data science. The paper outlines the assumptions made in coming to the conclusions reached by these investigators. They looked at breast, cervix, colorectal, lung, and prostate cancers — obviously, major cancers — and specifically looked at what the impact has been over the past 45 years of these three different strategies in averting deaths: prevention, screening, and actual treatment. The bottom line, as reported by these investigators, is that over this 45-year period, 5.94 million deaths have been averted in these five cancers combined, due to the efforts of countless numbers of individuals, researchers, clinicians, public health officials, government regulators, etc. It's an incredible and an enormously positive contribution to society and to individual patient health. They note, and this is a powerful message, that 8 of the 10 deaths, 80%, that had been averted were due to efforts in cancer prevention and screening. It may come as a surprise to some, but not to all, because of our often very intense focus and money spent on treatments for established and advanced cancers over the past decades. There's no intent either in this paper or by me to denigrate — in any way, shape, or form — the enormous efforts that have been made in treatment. But if you look at the question of deaths averted, the vast majority have come from prevention and screening efforts. And clearly, there's cost involved in these efforts, but far less than that associated with development of treatments. They're even more specific in this paper: Screening, according to these investigators, has been responsible for essentially all reduction in cervix cancer, which we certainly know from the enormous contributions of the Pap smear screening and now HPV screening: 25% of breast cancer deaths were averted due to screening; 56% from prostate cancer; 79% of deaths from colorectal cancer; and, of course, from lung cancer, 98% of the impacts on cancer deaths has resulted from a reduction in smoking. So, overall a tremendous impact, a positive impact. So many individuals and organizations avert deaths, but it's critical to remember the role of prevention and screening. And as we move forward to the future, as we look at the epidemic we have of obesity in this country and the concern about the risk of alcohol on the risk for cancer, it is important to remember the critical role to the present but also for the future of prevention and screening. Thank you for your attention.
Yahoo
3 days ago
- Health
- Yahoo
Opinion - The ugly truth about the student loan caps in Trump's ‘big beautiful' law
New federal student loan caps pose an urgent and overlooked threat to the health of all Americans. These changes will severely undermine the graduate education pipeline for the clinician workforce — including both nurses and physicians— jeopardizing access to care, straining the workforce and, ultimately, harming patients. The bill, now signed into law, will cap graduate unsubsidized student loans at $20,500, with a $100,000 total cap on top of undergrad loans, and phase out Grad PLUS loans. These changes are especially detrimental for those pursuing clinician roles, such as nurse practitioners. Nurse practitioners play a crucial role, filling gaps in primary care — especially in rural and underserved communities. Their presence expands access, relieves pressure on healthcare systems and allows physicians to focus on the most complex cases. Graduate education is not optional for becoming a nurse practitioner. Nor is it optional for becoming faculty to teach the next generation of physicians and nurses. Weakening the pipeline of advanced practice nurses doesn't just hurt nursing, it threatens the entire care delivery system. For nursing, this is a moment where education is already strained. Nurses have left the profession en masse since the COVID-19 pandemic and older nurses are retiring. We urgently need more nurses and nurse educators in the pipeline. Yet in 2023, enrollment in bachelor's-level nursing programs grew by just 0.3 percent. Meanwhile, enrollment in master's and Ph.D. nursing programs declined by 0.9 percent and 3.1 percent, respectively. That same year, U.S. nursing schools turned away more than 65,000 qualified applications due to a lack of faculty, clinical placements and funding — not because of a lack of interest. Faculty shortages are especially dire. Nearly 2,000 full-time faculty vacancies remain unfilled nationwide, according to the American Association of Colleges of Nursing. These positions require a master's or doctoral degree — precisely the kind of education now placed at risk by this legislation. Without nurse educators, we cannot train the next generation of nurses at any level. This law also directly contradicts the Make America Healthy Again initiative, which calls on healthcare systems to take on chronic disease through prevention. Nurses make up the largest segment of the healthcare workforce. Their education emphasizes prevention and whole-person care for people and communities. Nurses are central to the shift from reactive 'sick care' to proactive prevention, so restricting their ability to enter the profession is not just shortsighted, it's self-defeating. A diminished nursing workforce will trigger a familiar cycle: reduced access, longer wait times, more chronic disease and an even more overwhelmed workforce. And these consequences won't be limited to nurses — they will affect physicians, hospitals, insurers and, most of all, everyday Americans. This is a national health issue. While the bill has passed, it is not too late to mitigate its harm. Policymakers must find alternative solutions, from scholarship expansion to loan forgiveness, to ensure access to graduate nursing education remains within reach. We cannot solve a workforce shortage and a chronic disease crisis by cutting off the professionals trained to fix it. Sarah Szanton is dean of the Johns Hopkins School of Nursing. Copyright 2025 Nexstar Media, Inc. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed. Solve the daily Crossword
Forbes
4 days ago
- Health
- Forbes
Rethinking Work With AI: What Stanford's Groundbreaking Workforce Study Means For Healthcare's Future
AI systems should reduce cognitive load, clarify ambiguity, and work alongside teams as intelligent collaborators, not as black-box disruptors. What if the AI systems you're building solve the wrong problems and alienate the workforce you're trying to support? That's the uncomfortable reality laid bare by a new research study from Stanford University. While AI pilots race ahead across administrative and clinical functions, most are still built on a flawed assumption: that automating tasks equals progress. But for the people doing the work—clinicians, care coordinators, billing specialists—that's not what they asked for. The report, Future of Work with AI Agents, offers the most granular audit yet of how worker sentiment, task complexity, and technical feasibility collide in the age of artificial intelligence. Over 1,500 U.S. workers were surveyed across 104 occupations, producing the most detailed dataset yet on where AI could, and should, fit. Their preferences were paired with ratings from 52 AI experts to create a map of the true automation and augmentation landscape. For healthcare, the findings could not come at a more urgent moment. The healthcare sector faces a burned-out workforce, escalating administrative waste, and widespread dissatisfaction with digital tools that were meant to help. A majority of physicians report that documentation burden is a leading cause of burnout, with recent studies showing U.S. physicians spend excessive time on documentation tasks. Nurse attrition has also remained a concern since the pandemic. Meanwhile, AI adoption is surging, with the vast majority of health systems piloting or planning AI integration. However, there remains a lack of consistent frameworks to align these technologies with real-world clinical and operational dynamics. The result? Misplaced investment, fractured trust, and resistance from the very people AI is meant to assist. The Stanford study confirms it: the majority of tasks that healthcare workers want automated—like documentation, claims rework, or prior auth form generation—are not where AI tools are being focused. In fact, less than 2% of those high-desire tasks are showing up in actual LLM usage today. Instead, attention and venture funding are often diverted toward automating interpersonal communication, appeals, or triage. These are areas where trust, nuance, and empathy matter most. This is more than a technical oversight. It's a strategic miscalculation. This study clarifies that the future of AI in healthcare isn't about replacing human judgment—it's about protecting it. Leaders must pivot from automation-at-any-cost to augmentation-by-design. That means building AI systems that reduce cognitive load, clarify ambiguity, and work alongside teams as intelligent collaborators, not as black-box disruptors. And, most critically, it means listening to the workforce before you deploy. A New Lens on Work: Automation Desire vs. Technical Feasibility Stanford's framework introduces two powerful filters for every task: what workers want automated and what AI can do. This produces a four-quadrant map: This approach is especially revealing in healthcare, where: Critically, 69% of workers said their top reason for wanting AI was to free up time for higher-value work. Only 12% wanted AI to fully take over a task. The takeaway? Augmentation, not replacement. Green Light (Automate Now): R&D Opportunity (Invest in Next-Gen AI): Red Light (Approach with Caution): Y Combinator is one of the world's most influential startup accelerators, known for launching and funding early-stage technology companies, including many that shape the future of artificial intelligence. Its relevance in this context comes from its outsized role in setting trends and priorities for the tech industry: the types of problems YC-backed startups pursue often signal where talent, investment, and innovation are headed. The Stanford study highlights a striking disconnect between these startup priorities and actual workforce needs. Specifically, it found that 41% of Y Combinator-backed AI startups are developing solutions for tasks that workers have little interest in automating—referred to as 'Red Light Zones' or low-priority areas. This reveals a substantial missed opportunity: if leading accelerators like Y Combinator better aligned their focus with the real needs and preferences of the workforce, AI innovation could deliver far greater value and acceptance in the workplace. The Human Agency Scale: AI as a Teammate To move beyond binary thinking (automate vs. don't), the Stanford research team introduces a more nuanced framework: the Human Agency Scale (HAS). This five-tier model offers a conceptual scaffold for evaluating how AI agents should integrate into human workflows. Rather than asking whether a task should be automated, the HAS asks to what extent the human remains in control, how decision-making is shared, and what level of oversight is required. The scale ranges from H1 to H5, as follows: The Stanford study reveals a clear pattern across occupations: the majority of workers—particularly in healthcare—prefer H2 or H3. Specifically, 45.2% of tasks analyzed across all industries favor an H3 arrangement, in which AI acts as a collaborative peer. In healthcare contexts—where judgment, empathy, and contextual nuance are foundational—H3 is even more critical. In roles such as care coordination, utilization review, and social work, tasks often require a mix of real-time decision-making, human empathy, and risk stratification. A system built for full automation (H5) in these contexts would not only be resisted—it would likely produce unsafe or ethically problematic outcomes. Instead, what's required are AI agents that can surface relevant information, adapt to the evolving contours of a task, and remain responsive to human steering. John Halamka, President of Mayo Clinic Platform, reinforced this collaborative mindset in February 2025: 'We have to use AI,' he said, noting that ambient listening tools represent 'the thing that will solve many business problems' with relatively low risk. He cited Mayo's inpatient ambient nursing solutions, which handle '100% of the nursing charting without the nurse having to touch a keyboard,' but was clear that these tools are 'all augmenting human behavior and not replacing the human.' These insights echo a broader workforce trend: automation without agency is unlikely to succeed. Clinical leaders don't want AI to dictate care pathways or handle nuanced appeals independently. They want AI that reduces friction, illuminates blind spots, and extends their cognitive reach, without erasing professional identity or judgment. As such, designing for HAS Level 3 (equal partnership) is emerging as the gold standard for intelligent systems in healthcare. This model balances speed and efficiency with explainability and oversight. It also offers a governance and performance evaluation framework that prioritizes human trust. Building AI for HAS Level 3 requires features that go beyond prediction accuracy. Systems must be architected with: Healthcare doesn't need one-size-fits-all automation. It requires collaboration at scale, grounded in transparency and guided by human expertise. These perspectives align perfectly with the Stanford findings: workers don't fear AI—they fear being sidelined by it. The solution isn't to slow down AI development. It's to direct it with clarity, co-design it with the people who rely on it, and evaluate it not just by outputs but also by the experience and empowerment it delivers to human professionals. The true ROI of AI is trust, relief, and time reclaimed. Outcomes like 'claims processed' or 'notes generated' aren't enough. Metrics should track cognitive load reduced, time returned to patient care, and worker trust in AI recommendations. While throughput remains a necessary benchmark, these human-centered outcomes provide the clearest signal of whether AI improves the healthcare experience. Measurement frameworks must be longitudinal, capturing not just initial productivity but long-term operational resilience, clinician satisfaction, and sustainable value. Only then can we ensure that AI fulfills its promise to elevate both performance and purpose in healthcare. Dr. Rohit Chandra, Chief Digital Officer at Cleveland Clinic, gave voice to this idea in June 2025: 'It's made their jobs a ton easier. Patient interactions are a lot better because now patients actually engage with the doctor,' he said, referring to 4,000 physicians now using AI scribes. 'I'm hoping that we can keep building on the success that we've had so far to literally drive the documentation burden to zero.' Build With, Not For This moment is too important for misalignment. The Stanford study offers a blueprint. For healthcare leaders, the message is clear: If you want AI to scale, build with the workforce in mind. Prioritize the Green Light Zones. Invest in agentic systems that enhance, not override. Govern AI like a trusted partner, not a productivity engine. The future of AI in healthcare won't be determined by the size of your model. It will be defined by the quality of your teaming.
