Sleep and Parkinson's Disease: Webinar at Michael J Fox Foundation

Michael J Fox Foundation holds monthly webinars; here AI notes on a recent session on sleep disorders in PD.

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 https://www.michaeljfox.org/webinars

https://www.michaeljfox.org/webinar/sleep-and-parkinsons-whats-going-and-what-can-help

Soania Mathur MD / MJFF Patient Council

Wanda Kim Lilly / Patient / MJFF Patient Council

Emmanuel During MD / Icahn School of Medicine / Mt Sinai / NYC

Lkeanis Vaou MD, FAAN, Univ Texas San Antonio

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This Michael J. Fox Foundation webinar on sleep in Parkinson’s disease brings together a moderator with Parkinson’s, a patient advocate, and two physician experts in movement disorders and sleep medicine to explain why sleep problems are so common in Parkinson’s, what kinds of problems occur, and what can actually help. The panel makes the point that sleep is not a side issue in Parkinson’s. It is a major part of daily functioning, quality of life, and even brain and body health. Good sleep supports brain “reset,” toxin clearance, immune function, physical recovery, metabolism, and emotional regulation, while both too little and too much sleep can be harmful. They describe normal sleep as a cycling process through deep sleep and REM sleep across the night, with deep sleep tending to dominate earlier and REM later.

A major theme of the webinar is that sleep problems in Parkinson’s are common, varied, and often under-discussed in clinic. The experts emphasize that many patients do not spontaneously report nighttime symptoms unless asked directly, and that clinicians may fail to ask. The most common complaint is sleep maintenance insomnia rather than difficulty falling asleep: people with Parkinson’s often wake repeatedly through the night, sometimes six to eight times, for different reasons. Those reasons may include pain, muscle cramps, difficulty turning over in bed, nighttime “wearing off” of dopamine medication, tremor, restless legs, frequent urination, anxiety, sleep apnea, or REM sleep behavior disorder. A particularly useful point is that the panel does not present “Parkinson’s insomnia” as one single thing. Instead, they urge patients and doctors to tease apart the causes, because treatment depends on identifying what is actually waking the person up.

The patient panelist gives a vivid real-world account of how this can feel. She says she used to be an excellent sleeper, but later developed painful muscle cramps and dystonia, including leg cramps at night. What woke her up was the pain, but what kept her awake was fear—the fear that a new symptom meant disease progression or loss of control. That distinction becomes one of the webinar’s most human and practical insights: in Parkinson’s, disrupted sleep can become a feedback loop of symptom, vigilance, and anxiety. The panel repeatedly returns to this idea, noting that once a person starts expecting poor sleep, that expectation itself can help perpetuate insomnia.

The webinar also explains why Parkinson’s affects sleep biologically, while cautioning that not every sleep complaint is directly caused by the disease itself. One expert says Parkinson’s and other neurologic disorders can disturb the brain systems that regulate sleep and wakefulness, but also stresses that many contributors are treatable coexisting sleep disorders or behavioral factors. This is especially important because patients may assume poor sleep is simply “part of Parkinson’s” and therefore unavoidable. The experts push back against that resignation. They say that even if sleep is not perfect, it can usually be improved, and that patients should not fixate on the idea that nothing can be done. They also note that aging itself fragments sleep, so not every nighttime awakening is uniquely Parkinsonian.

A centerpiece of the discussion is REM sleep behavior disorder, or RBD, which the presenters describe as one of the most distinctive sleep disorders associated with Parkinson’s. In normal REM sleep, the brain is active and dreaming, but the muscles are effectively paralyzed or “locked” so the person does not physically act out dreams. In RBD, that locking mechanism fails, allowing people to twitch, yell, punch, kick, or otherwise enact dreams. The expert explains that the relevant brainstem circuitry is often affected very early in Lewy body disease, sometimes years before classic Parkinsonian motor symptoms appear. About half of patients may develop these symptoms before tremor or movement problems, making RBD not just a symptom but also a potential early marker of elevated Parkinson’s risk. That is one reason it is such an important focus for research.

The panel repeatedly stresses the value of care partners or bed partners in recognizing sleep disorders. Patients may not know they snore, stop breathing, or act out dreams because they are asleep when it happens. Care partners can report snoring, gasping, witnessed apneas, screaming, punching, dream enactment, and other nighttime behaviors that are diagnostically crucial. This is particularly relevant for RBD and sleep apnea, both of which can go unrecognized unless someone else observes them. The message is that sleep history in Parkinson’s should be gathered from both the patient and, when possible, the person sharing the room or bed.

On the practical side, the webinar gives a strong endorsement of sleep hygiene and lifestyle measures before defaulting to sleeping pills. The experts recommend consistent sleep and wake times, avoiding long daytime naps, exercising regularly, limiting alcohol and heavy meals before bed, keeping the bedroom cool and dark, minimizing light exposure at night, and getting daylight exposure during the day. One sleep specialist gives a particularly concrete example of a patient with Parkinson’s whose sleep improved markedly just by following these recommendations: setting a regular schedule, reducing anxiety, exercising more, lowering the bedroom temperature, and changing beliefs about sleep. The panel frames this as encouraging but also realistic: these habits work, but they require discipline and can be hard to sustain. They compare adherence to sleep hygiene to starting a diet—simple in theory, difficult in practice, but often effective when maintained.

The patient advocate adds a nice layer of self-management detail. She keeps a journal tracking symptoms and possible triggers. From observation, she learned that sugar, alcohol, inadequate hydration, and being physically cold at bedtime seemed to provoke cramps. She also found that direct heat, especially an old-fashioned hot water bottle, helped reduce recurrent cramps and eased the fear that another cramp was about to start. Most importantly, she deliberately changed her mental framing: instead of treating poor sleep as something catastrophic or life-limiting, she chose to see it as something that could be improved. That blend of practical adjustment and cognitive reframing is presented as a meaningful part of coping.

The webinar gives a useful explanation of sleep studies. The experts distinguish between the traditional in-lab polysomnogram, which records brain waves, breathing, oxygen, heart activity, muscle activity, and video/audio overnight, and a home sleep test, which is simpler and more comfortable but usually answers only one question: whether the person has sleep apnea. The in-lab test is more comprehensive and can detect conditions like RBD in addition to apnea, but it is more cumbersome and expensive, and some people understandably sleep poorly in that setting. The home test is easier but more limited. This explanation helps demystify why one patient might be sent for one kind of study rather than the other.

On treatment, the physicians are cautious about reflexively prescribing generic sleep aids. They say that in Parkinson’s, the better approach is often to identify the specific source of the disruption and treat that. For example, cramps, painful rigidity, trouble turning in bed, and restless discomfort may reflect overnight wearing-off of dopaminergic therapy. In those cases, they often consider nighttime extended-release carbidopa/levodopa or dopamine agonists, because patients still need dopamine coverage while asleep. One expert also says that deep brain stimulation (DBS) often improves sleep indirectly by providing continuous overnight control of motor symptoms, even though the precise effects on sleep circuitry remain an area of research. Patients frequently report that after DBS they sleep better, even if sleep was not the original treatment target.

When medications specifically for sleep are discussed, the experts mention a few options but still present them as secondary to careful assessment. One speaker highlights orexin antagonists as a newer class that can improve sleep without being habit-forming, and also mentions trazodone as an older medication that can be quite helpful in some patients, especially by supporting deeper sleep early in the night. The tone is not anti-medication, but it is distinctly anti-quick-fix. Medication is treated as one tool among several, not the whole strategy.

The Q&A section covers several common questions. On melatonin, one doctor says it is often more useful for REM sleep behavior disorder than for ordinary insomnia. Patients may assume melatonin is being prescribed simply to help them sleep, but the expert says she more often uses it to reduce dream enactment behaviors. Another expert adds that with melatonin, more is not necessarily better, and that taking it at the same clock time each evening may be more important than taking high doses, because of its role in regulating circadian rhythm. On magnesium, the transcript references it mainly in the context of the patient’s cramps rather than as a broad sleep cure.

The webinar also addresses napping, which is handled with nuance rather than dogma. The recommendation is not “never nap,” but rather: if you truly need one, keep it short—about 30 minutes or less—because shorter naps are more refreshing and less likely to interfere with nighttime sleep. Longer naps may leave people groggy and reduce sleep drive for the next night. If a care partner notices someone has been napping too long, a gentle awakening, followed by activity or a walk outside, may help reestablish alertness.

Another practical symptom discussed is nighttime temperature dysregulation—waking up sweaty one moment and freezing the next. The expert links this to autonomic dysfunction in Parkinson’s, especially in the setting of medication wearing off. Suggestions include adjusting overnight Parkinson’s treatment and using simple supportive strategies such as warm socks or thermal clothing when cold extremities are part of the problem. Again, the webinar’s approach is to connect the symptom back to Parkinsonian physiology without assuming there is a single uniform fix.

The research portion is notably optimistic. One expert is especially interested in ways to enhance deep sleep and in the use of wearable devices and AI-based analysis to detect subtle movements during REM sleep that may identify RBD—and therefore elevated Parkinson’s risk—years before motor diagnosis. The idea is that consumer-style sleep devices might someday become scalable tools for earlier detection of neurodegenerative disease. The panel also promotes participation in PPMI, the Parkinson’s Progression Markers Initiative, as well as other research opportunities, arguing that progress depends on large-scale patient participation and long-term data collection.

Overall, the webinar’s message is both practical and hopeful. Sleep disturbance in Parkinson’s is common and complicated, but it is not something patients should silently endure or dismiss as untreatable. The panel urges people to tell their clinicians about sleep symptoms, involve care partners in reporting nighttime behaviors, improve sleep hygiene, look for specific treatable causes, and seek a sleep specialist when needed. The closing tone is realistic but upbeat: sleep may not become perfect, but in many cases it can become meaningfully better, and better sleep can make living with Parkinson’s better too.

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If of interest, see also a 2020 paper by Pfeiffer on autonomic dysfunction in PD: PMID: 32789741

https://doi.org/10.1007/s13311-020-00897-4

Profiling Indiana Univ Prof. Jennifer Oliva: AI in Healthcare and More

 An April 2026 STAT PLUS article on United Healthcare and AI highlighted the expertise of Prof. Jennifer Oliva of Indiana University.   Article by Casey Ross.

Here, Chat GPT summarizes some of her work.  Find her bio here which includes comprehensive links to her publications.

https://law.indiana.edu/about/people/details?name=oliva-jennifer-d

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Professor Jennifer D. Oliva emerges from these materials as a health-law scholar working at the junction of AI, insurance coverage, public health, and administrative power. Her Indiana bio places her at Indiana University Maurer School of Law as Professor of Law and Val Nolan Faculty Fellow, with research interests spanning health law and policy, privacy, evidence, torts, and complex litigation.  Her bio also shows a notably interdisciplinary background—West Point, Oxford MBA, Georgetown JD—plus roles with Georgetown’s O’Neill Institute and the UCSF/UC Law Consortium.

What is striking in Oliva’s recent work is that she does not treat AI in healthcare as a generic “innovation” story. She treats it as a power-allocation problem: who gets to decide, at scale and often opaquely, whether patients receive care, whether agencies remain evidence-based, and whether the law can still reach the real actors making consequential decisions. That theme runs through both her insurance-algorithm articles and, in a different register, through “Government Goes Goop.”

In “Regulating Healthcare Coverage Algorithms” (Indiana Law Journal, 2025), Oliva’s basic move is to shift the center of attention from clinical AI to coverage AI. She notes that while FDA regulates many AI-enabled clinical tools, insurers also use algorithms to determine whether care is “medically necessary” and how much care will be covered, yet those coverage algorithms remain largely unregulated, proprietary, and shielded from external validation. She argues that this is not a merely administrative issue: coverage algorithms can be used to delay or deny medically necessary treatment, with direct consequences for patient health.

[The Biden administration proposed a rule in late 2024 that would have required Medicare Advantage plans to  have much higher clarity about AI and coverage criteria in general; this was nixed in the final rule under Trump II.]

That article presents Oliva as a scholar with a very clear instinct: follow the real decision-maker. If an algorithm is effectively deciding access to care, she argues, then the law should not be distracted by formal distinctions between a tool that guides treatment and a tool that governs payment for treatment. Her argument is that those distinctions may look neat on paper, but in the real world, where most patients cannot self-fund expensive care, a coverage algorithm can be just as consequential as a diagnostic or treatment algorithm. 

On that basis, she presses for robust oversight, ideally through FDA authority if available, and otherwise through legislative expansion and interim state action requiring pre-market assessment for validity, accuracy, and fairness.

The article’s tone is also important. It is not technophobic. Oliva acknowledges that such tools may promise efficiency and standardization. But she is skeptical of the way those promises interact with insurer incentives. Her recurring concern is that AI, when deployed inside utilization management, can become a mechanism for industrialized claims control rather than improved care. In her framing, the real policy problem is not only bias or opacity in the abstract, but the combination of automation plus profit motive plus weak oversight.

Her later article, “Regulating Healthcare Coverage Algorithms in the Shadow of ERISA” (Michigan Law Review, forthcoming 2027), sharpens and advances that project. Here, Oliva takes up the big doctrinal obstacle: even if states want to regulate these systems, won’t ERISA preemption block them? 

Her answer is the article’s central intellectual contribution. She argues that states should reconceive coverage algorithms not as inseparable parts of employee benefit plan administration, but as standardized commercial products designed, manufactured, and sold by third-party vendors. If that is right, then state rules requiring validation of these tools are better understood as product safety regulation, not forbidden interference with plan administration.

That is a clever and important pivot. Instead of attacking ERISA head-on, Oliva tries to route around it. She accepts that ERISA has long frustrated state regulation of employer-sponsored health plans, especially self-insured plans, but argues that states still retain room to regulate the software products themselves. The article therefore proposes a model state framework centered on pre-market validation, ongoing performance monitoring, and enforcement by specialized state Algorithm Policy Offices, with regulation directed at vendors rather than plans.

So the difference between the two algorithm papers is useful. The Indiana piece is the broad normative and regulatory claim: these coverage algorithms are high-stakes healthcare tools and should not enjoy a “free ride.” The Michigan piece is the doctrinal and institutional sequel: given the constraints of ERISA and federal inaction, here is a legally defensible path for state governance. Together, they show Oliva at work as both critic and constructor—first identifying the regulatory void, then designing a plausible architecture to fill it.

The ERISA article also shows another feature of her style: she writes against the grain of conventional assumptions. The abstract expressly says the article “challenges” the assumption that comprehensive state oversight is beyond reach because of ERISA. That tells you something about her scholarly temperament. She does not simply describe preemption as an immovable barrier; she treats it as a legal terrain that can be reinterpreted for the era of algorithmic decision-making.

Then there is “Government Goes Goop” (Emory Law Journal Online, 2026), which at first looks like a departure from AI-insurance scholarship but in fact fits the same larger pattern. Here Oliva argues that the rise of wellness and antivaccine figures into senior federal health roles represents the culmination of a long historical evolution in American health fraud—from medicine shows to institutional capture. She traces continuities in tactics: emotional manipulation, conspiratorial framing, anti-establishment posture, and exploitation of information asymmetries.

The paper is especially pointed in its treatment of Trump Administration 2. Its table of contents and introduction frame the administration’s health leadership as a “wellness cabinet,” with discussions of Kennedy at HHS, Bhattacharya at NIH, Oz at CMS, and Makary at FDA, plus subsequent vaccine-skeptic appointments. Oliva’s claim is not merely that these figures hold controversial views. It is that federal health agencies risk being transformed from evidence-based institutions into platforms for wellness ideology, with effects including staff departures, preventable outbreaks, and weakened scientific credibility.

What links “Government Goes Goop” to the insurance-algorithm work is her deeper preoccupation with epistemic governance. In one set of papers, the question is: who validates the algorithm that determines care? In the Goop paper, the question becomes: who validates the very institutions meant to protect scientific standards? In both settings, Oliva worries about systems that look official, scalable, and rationalized, yet may be driven by commercial incentives, ideology, or both, while ordinary patients bear the risk.

A fair overall profile, then, is that Oliva is developing into a scholar of health-law infrastructure. She studies not just rights or doctrines in isolation, but the machinery by which modern healthcare decisions are made: utilization-management software, regulatory jurisdiction, preemption doctrine, agency leadership, and the porous boundary between public health expertise and commercialized misinformation. Her work is distinctive because it combines practical policy urgency with doctrinal inventiveness. She is not content to say that AI and healthcare are complicated. She asks, very concretely, who is governing whom, by what tool, under what legal authority, and with what accountability.

 

World Parkinson Day at Cedars Sinai Los Angeles (April 11 2026)

 Revised Meeting Report

World Parkinson Day Community Workshop
Cedars-Sinai Medical Center, Los Angeles
April 11, 2026

At Cedars-Sinai’s April 11, 2026 Parkinson’s community workshop, speakers stressed that Parkinson’s extends far beyond tremor, spanning motor, non-motor, cognitive, and autonomic symptoms. The program reviewed newer treatments, remote digital monitoring, active clinical trials, atypical parkinsonism, and the growing role of palliative care. A closing presentation emphasized that surgery can help selected arm-and-leg motor symptoms, but not most midline or non-motor problems. Overall, the meeting offered a practical, hopeful roadmap for individualized multidisciplinary care. 

Video Archive

https://vimeo.com/1183179155/363e4c2b21?share=copy&fl=sv&fe=ci

The Cedars program director, Dr Tagliati, wrote Parkinson Disease for Dummies, which has excellent reviews.

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Cedars-Sinai’s Parkinson’s Patient Community Conference was held on Saturday, April 11, 2026, from 9:00 a.m. to 1:30 p.m. as a free hybrid event for patients with Parkinson’s disease and their caregivers. The published faculty included Michele Tagliati, John Mason, Echo Tan, Elliot Hogg, Yvette Bordelon, Jessica Besbris, Adam Mamelak, and Chae Kim. In his opening remarks, Dr. Tagliati noted that this was the 16th consecutive year Cedars-Sinai had organized its patient educational symposium, emphasizing continuity, education, and community support.

The workshop’s central message was that Parkinson’s disease is far more complex than tremor alone. Across the morning, speakers described Parkinson’s as a chronic, fluctuating, multidimensional illness involving motor symptoms, non-motor symptoms, treatment timing, monitoring challenges, research opportunities, atypical syndromes, supportive care needs, and surgical options. The tone was practical and hopeful: the meeting did not promise a cure, but it repeatedly stressed that care is becoming more individualized, data-informed, and multidisciplinary.

Dr. John Mason opened the educational content with a clear overview of the motor symptoms of Parkinson’s disease. He emphasized that Parkinson’s is heterogeneous, meaning patients do not all look alike and do not all share the same dominant symptoms. He reviewed bradykinesia, tremor, rigidity, dystonia, gait changes, freezing of gait, postural changes, postural instability, eye movement abnormalities, speech and swallowing problems, and later-stage dyskinesias. His presentation translated clinical language into daily life: smaller handwriting, difficulty buttoning clothing, reduced arm swing, softer speech, swallowing problems, and falls. He also made the important point that not every patient has major tremor, and that levodopa should not be delayed simply out of fear of dyskinesias, since dyskinesias are more tied to disease progression than to having started the drug “too early.”

Dr. Chae Kim followed with a broad review of non-motor symptoms, arguing that the classic motor picture is only the tip of the iceberg. She highlighted constipation, insomnia, REM sleep behavior disorder, anxiety, depression, apathy, cognitive changes, psychosis, fatigue, urinary symptoms, orthostatic hypotension, and temperature dysregulation. One of her most important points was temporal: several non-motor symptoms can begin years before the motor diagnosis, including constipation, REM sleep behavior disorder, and smell loss. She also emphasized that many patients experience these symptoms as more burdensome than tremor or stiffness. Her treatment discussion was broad and practical, spanning medication choices, sleep studies, bowel regimens, exercise, psychotherapy, attention to mood, and strategies for orthostatic hypotension. In the discussion afterward, she and Dr. Tagliati clarified that orthostatic hypotension is not usually “cured,” but it can often be managed effectively.

Dr. Michele Tagliati then shifted the focus toward digital biomarkers and remote therapeutic monitoring. His core argument was that modern medicine is optimized for acute illnesses, whereas Parkinson’s disease is chronic, variable, and context-dependent, making short office visits a poor fit as the sole basis for decision-making. He pointed to the mismatch between a condition that fluctuates hour to hour and a care model based on a brief office snapshot every few months. He reviewed wearable and app-based systems and highlighted Cedars-Sinai’s pilot experience with smartphone-based monitoring, especially the Neu Health platform. He described a model in which patients perform brief structured tasks through a phone, allowing clinicians to monitor tremor, gait, balance, dexterity, voice, cognition, mood, sleep, pain, blood pressure, medication timing, and symptom fluctuations between visits. His theme was that Parkinson care should become less reactive and more proactive, with continuous information replacing guesswork based on memory alone. 

The workshop also included a broader update on clinical research, with Dr. Elliot Hogg presenting what he described as a whirlwind tour of active and emerging Parkinson’s trials. His conclusion was especially notable: he argued that the era of “levodopa-only” thinking is fading, and that the field is moving toward a much broader therapeutic future that includes symptomatic treatments, disease-modifying strategies, wearable-device studies, stem-cell work, and other novel approaches. In the audience discussion, he addressed GLP-1-related research, noting active interest in the field but no currently recruiting California GLP-1 Parkinson trial within the scope he reviewed, while mentioning ongoing or mixed results from trials elsewhere, including liraglutide-related work.

A nice community interlude came next, when the audience was introduced to PCLA, described as a nonprofit built by Parkinson’s patients and care partners, for Parkinson’s patients and care partners. The representative explained that the group provides support groups, informational seminars, and other community resources, including even a comedy show, all aimed at helping patients and families navigate the steep information and support curve of living with Parkinson’s. That moment reinforced that the conference was not just about expert lectures, but also about peer connection and navigation support.

The newly available Part C materially deepens the second half of the meeting.

Dr. Yvette Bordelon spoke on atypical parkinsonism, which she described as the “other part of the Parkinson family” that resembles Parkinson’s disease but differs in mechanism, prognosis, and management. She reviewed the terminology—atypical parkinsonism, Parkinson’s-plus syndromes, and the newer phrase Parkinson’s-like disorders—and stressed that these disorders share parkinsonian motor features such as stiffness and slowness but have important distinguishing characteristics. She specifically identified the four main atypical parkinsonian syndromes as progressive supranuclear palsy, corticobasal degeneration/corticobasal syndrome, multiple system atrophy, and dementia with Lewy bodies, while also noting drug-induced and vascular parkinsonism as related considerations. Her examples were clinically concrete: early falls and eye movement problems in progressive supranuclear palsy, marked asymmetry, apraxia, dystonia, and myoclonus in corticobasal syndrome, and prominent dysautonomia in multiple system atrophy. She also made an important translational point: progress in Parkinson’s research can help atypical syndromes, and vice versa.

Dr. Jessica Besbris then presented on palliative care, a topic she explicitly said is often misunderstood. Her talk was one of the most conceptually important additions in Part C. She pushed back against the idea that palliative care is only for cancer or only for the end of life, and instead defined it as an approach aimed at improving quality of life for patients and families facing serious illness by addressing symptoms, psychosocial and spiritual distress, future planning, and medical decision-making. She described palliative care as a team sport, involving physicians, nurses, advanced practice providers, social workers, chaplains, pharmacists, and others, all working together to support patients and care partners. Her phrase that best captured the talk was that palliative care helps people “live as well as they can for as long as they can.” She emphasized that these needs may begin at diagnosis, not just near death, and may rise and fall over the course of illness.

Dr. Besbris also made the discussion very practical. She explained that in clinic she may talk with patients about what worries them about the future, what they want to plan for, and how to build a kind of roadmap for the course of illness. That roadmap can support discussions about advance healthcare directives, naming a decision-maker, and clarifying what matters most to the patient. Over time, those conversations may extend to major decisions such as feeding tubes, skilled nursing placement, travel as mobility worsens, and, later in illness, transitions to hospice care. Importantly, she did not present this as abstract philosophy. She also summarized evidence that adding palliative care to usual neurological care improves quality of life, decreases symptom burden, including depression, anxiety, constipation, pain, and other non-motor symptoms, reduces caregiver anxiety, and increases completion of future-planning documents. She noted that Cedars has a dedicated neuro-palliative team and described it as part of the institution’s multidisciplinary Parkinson infrastructure.

The final presentation, as you noted, was Dr. Adam Mamelak’s recorded video talk on surgical therapies for Parkinson’s disease. Dr. Mamelak framed surgery not as a cure, but as another form of symptom modulation. He divided treatment into three broad categories: medications, electrical stimulation, and ablative techniques. For the purposes of this talk, he focused mainly on deep brain stimulation (DBS) and focused ultrasound, describing them as the principal surgical modalities currently used day to day. One of the clearest take-home messages from his talk was his simple “arms and legs” rule: surgery tends to help arm- and leg-related motor symptoms such as bradykinesia, rigidity, dystonia, dyskinesia, and tremor, but is much less effective for midline symptoms such as swallowing difficulty, balance impairment, freezing of gait, and certainly not for non-motor symptoms like constipation or sleep problems. That clarification is often exactly what patients need when considering intervention.

He then compared the advantages of the two main surgical strategies. DBS, in his account, is reversible, adjustable, and non-destructive, allowing clinicians to titrate stimulation parameters over time. The tradeoff is that it is still a true surgical procedure, involving implanted hardware and cranial access. By contrast, lesion-based therapies such as focused ultrasound and stereotactic radiosurgery can be rapid, may avoid some traditional surgical risks, and can sometimes be used in older patients or even in those on blood thinners, with symptom relief appearing quickly in some cases. Dr. Mamelak also reviewed the brain targets used for interventional therapy, noting in particular that the ventral intermediate nucleus of the thalamus is a classic target for tremor-dominant disease. Overall, his talk cast surgery as a powerful but selective tool whose value depends heavily on choosing the right patient, the right symptom target, and realistic expectations.

Taken together, the full corrected transcript shows a workshop with a very deliberate arc. It began with recognition of symptoms, moved into monitoring and treatment, widened into research and atypical syndromes, then expanded further into quality of life, planning, caregiver support, and finally surgical intervention. In that sense, the conference did more than teach facts. It modeled a modern Parkinson’s program as something broader than medication management: a system involving specialists, data tools, patient organizations, supportive care, multidisciplinary planning, and selected procedures.

Bottom line: with Part C now included, the conference reads even more clearly as a meeting about the whole Parkinson’s journey. Earlier talks explained the disease and its monitoring; the newly added talks showed how Cedars is also thinking about diagnostic nuance, life planning, caregiver burden, and targeted surgical intervention. The final message was not just that Parkinson’s is treatable, but that care improves when it becomes multidisciplinary, anticipatory, and honest about both possibilities and limits.

I can also turn this into a blog-style article with a 75-word top summary or a cleaner meeting memo format.

World Parkinson Day at UCLA (4 11 2026)

Based on YouTube archive.

https://www.youtube.com/watch?v=Mfia3ZAuc0c

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 Report: UCLA World Parkinson’s Day Symposium, April 11, 2026

Note: I standardized speaker names where they were identifiable from UCLA and trial sources; the source transcript you shared rendered several names phonetically. 

The UCLA Parkinson symposium was held on World Parkinson’s Day, which is observed each year on April 11. The event was framed by Dr. William Zeiger, a UCLA movement-disorders neurologist, and it reflected the broader work of UCLA’s Parkinson’s and movement-disorders research community within the Howard and Irene Levine Family Center for Movement Disorders.

What made the symposium effective was its architecture. It was not just a patient-education morning, and it was not just a research seminar. It was deliberately organized as a walk across the full Parkinson’s pipeline: basic disease mechanisms, protein misfolding, microglial biology, human gait circuitry, preclinical drug development, and finally active clinical trials. The result was a coherent picture of Parkinson’s disease not as a single narrow motor disorder, but as a long, slowly evolving, biologically diverse condition in which neurons, glia, proteins, environmental exposures, aging, and circuitry all interact.

Dr. Zeiger’s opening set the tone by translating technical vocabulary into plain language. He reviewed the basic cast of brain cell types—neurons, oligodendrocytes, astrocytes, and microglia—and emphasized that Parkinson’s cannot be understood only as a problem of dopamine neurons. He explained the familiar anatomy of the substantia nigra, the loss of pigmented dopamine-producing neurons, and the role of alpha-synuclein aggregation in forming Lewy bodies. This introductory section was modest in ambition but very important in function: it gave the audience a shared conceptual language for everything that followed.

The first major scientific lecture, from Dr. Jeff Bronstein, provided the symposium’s clearest statement of the current etiologic model of Parkinson’s disease. Bronstein argued that Parkinson’s is usually not caused by one thing, but by an accumulation of risk factors acting on a susceptible biological background. His framework combined rare high-impact mutations, common low-impact genetic polymorphisms, environmental toxicants, aging, inflammation, mitochondrial stress, and impaired protein-clearance pathways. He repeatedly returned to a central idea: Parkinson’s is likely a disorder that begins years to decades before diagnosis, with nonmotor symptoms such as constipation, smell loss, anxiety, dream-enactment behavior, and autonomic changes appearing well before tremor or bradykinesia.

Bronstein’s talk was also the symposium’s strongest reminder that association is not the same as causation. He reviewed epidemiologic links—smoking, alcohol, coffee, exercise, diet, pesticides, air pollution, solvents, head trauma—and used simple examples to show why correlations must be tested experimentally. That point gave his pesticide work unusual credibility. Rather than stopping at observational data, he described the UCLA strategy of identifying candidate exposures in human populations and then moving into animal models to test biologic plausibility. His discussion of chlorpyrifos was the key example: epidemiologic association first, then mouse and zebrafish experiments showing impaired movement, dopamine-cell injury, alpha-synuclein accumulation, inflammatory microglial changes, and disrupted intracellular “garbage disposal” pathways. Bronstein’s bottom line was practical as well as scientific: every patient’s Parkinson’s may have a somewhat different causal mix, but many overlapping risk modifiers—exercise, diet, avoidance of toxic exposures—remain meaningful even after diagnosis. Bronstein is director of UCLA’s movement-disorders program, and UCLA describes his work as focused on Parkinson’s causes and therapy development, including zebrafish models.

The next lecture, from Dr. Chao Peng, moved the audience from epidemiology into molecular strategy. Peng’s subject was alpha-synuclein as the central “bad actor” in Parkinson’s pathology: a normally useful protein that can misfold, template further misfolding, amplify itself, and spread from cell to cell. His lab focus at UCLA is precisely this terrain—pathological alpha-synuclein, its conformational diversity, and ways to interrupt it.

Peng’s presentation was one of the symposium’s most forward-looking. He described three therapeutic choke points: blocking fibril formation, blocking cell-to-cell transmission, and blocking amplification of pathology inside recipient cells. The most striking part was his discussion of AI-assisted drug design. Standard small-molecule discovery, he argued, is poorly suited to the unusual geometry of alpha-synuclein fibrils, which are not ball-like proteins with ordinary pockets but layered fiber structures with repeated binding surfaces. His lab’s innovation was to redesign the computational approach so that the AI would favor repeating, stackable molecules capable of interacting with repeated fibril layers. He paired that with high-throughput experimental validation in neuron cultures exposed to pathologic alpha-synuclein. The conceptual message was that AI is not being used here as a buzzword, but as a way to attack a structural problem that ordinary medicinal chemistry handles badly.

He then broadened the strategy by discussing mathematical modeling of how pathology spreads across connected brain networks, and by showing how regional vulnerability can suggest new drug targets. Finally, he described work on post-translational modifications of soluble alpha-synuclein—small chemical “tags” that can either worsen or restrain pathologic conversion. This part of the symposium was especially important because it implied that treatment may not come from one blunt anti-synuclein approach, but from multiple more precise interventions tailored to different strains, conformations, or amplification states.

The third talk, from Dr. Lindsay De Biase, shifted the discussion from neurons to microglia, and in some ways deepened the entire symposium. UCLA describes De Biase’s work as centered on microglia and their role in neuroinflammation and aging-related vulnerability.

De Biase’s core argument was that Parkinson’s research has historically centered too narrowly on neurons, when in fact half the cells in the brain are non-neuronal, and microglia in particular may shape which neurons become vulnerable, when, and why. She explained microglia both as the brain’s “immune” cells and as active regulators of synapses, excitability, and tissue health. Her most memorable data concerned regional differences: in dopamine-rich midbrain regions, microglia appear to be fewer in number, less branched, and to have fewer lysosomes than in some neighboring regions. That matters because lysosomes are the cell’s degradative machinery. During aging, those lysosomes become overloaded with damaged proteins and lipids, microglia proliferate, inflammatory signaling rises, and local dopamine circuits perform worse. She then added a hopeful twist: microglia may also physically contact and protect dopamine neurons, and more such contact was associated with better behavioral performance in aging mice. De Biase’s talk gave the symposium one of its most important conceptual upgrades: Parkinson’s progression may depend not only on toxic proteins but on the state of the surrounding glial environment.

After the break, Dr. Kathryn (“Katy”) Cross brought the discussion into human physiology. UCLA describes her lab as studying gait impairment and human brain-circuit abnormalities in Parkinson’s disease, using tools such as virtual reality, EEG, motion capture, DBS recordings, and other neural measurements.

Cross’s lecture was excellent because it showed why walking is such a hard symptom to treat. Walking is not a single output; it is a constantly updated negotiation among rhythm, balance, visual input, cortical planning, and basal-ganglia “autopilot.” In Parkinson’s, especially in freezing of gait, that negotiation breaks down. Her group’s solution is to study walking while it is actually happening, not only in seated scans. She described mobile EEG, motion sensors, DBS recordings, eye tracking, and especially virtual reality designed to trigger freezing episodes in realistic but controlled settings. This was a very translational talk: the point is not merely to observe freezing, but to identify the exact brain signals that could someday guide adaptive stimulation or more targeted noninvasive neuromodulation. Cross’s contribution made clear that gait failure is not peripheral or secondary. It is one of the clearest demonstrations that Parkinson’s is a circuit disorder.

Next, Dr. Gal Bitan discussed the long arc of preclinical drug development. UCLA identifies Bitan’s lab with the development of molecular tweezers, especially the compound CLR01, as inhibitors of abnormal protein aggregation.

Bitan’s talk was perhaps the most concrete illustration of how a laboratory idea becomes a drug candidate. He walked the audience through the sequence: efficacy in test-tube aggregation assays, cell-culture toxicity rescue, zebrafish benefit, mouse-model benefit, toxicology, pharmacokinetics, and finally startup-company formation. His molecular tweezers do not eliminate alpha-synuclein; rather, they appear to redirect it away from the most toxic forms and to accumulate in lysosomes, where alpha-synuclein degradation is under pressure. This tied his talk elegantly back to De Biase’s lysosomal story. The audience could see, maybe more vividly than anywhere else in the symposium, how basic biophysics, animal modeling, and commercial translation fit together.

The symposium ended with Dr. Danielle Thordarson, a UCLA neurologist focused on movement disorders and Parkinson’s disease, who reviewed the current clinical-trials landscape. Her talk was valuable because it translated the morning’s science into near-term opportunities for patients. She emphasized that current Parkinson’s drugs remain mainly symptomatic, while the field is pushing toward disease modification.

She highlighted three especially important trial themes. First was prasinezumab, the anti-alpha-synuclein antibody now in Roche’s global Phase 3 PARAISO study for early-stage Parkinson’s disease. Second was NEU-411 in the Phase 2 NEULARK study for LRRK2-driven Parkinson’s disease, representing a more precision-based strategy. Third was bemdaneprocel, BlueRock’s stem-cell-derived cell therapy in the exPDite-2 study, a major effort to replace lost dopaminergic function. These trials are publicly listed as active investigational programs.

The larger achievement of the symposium was not that it offered a single answer. It did the opposite, and that was its strength. It showed Parkinson’s disease as a plural problem: partly proteinopathy, partly inflammatory disorder, partly aging disorder, partly circuit disorder, and partly an individualized biologic syndrome in which different patients may need different combinations of therapy. Across the talks, a common theme emerged: the future of Parkinson’s treatment will likely be layered. It may involve anti-synuclein strategies, microglial or lysosomal modulation, precision genetic therapies, circuit-guided stimulation, rehabilitation tools, and possibly restorative cell therapy. The symposium therefore succeeded not by promising a cure tomorrow, but by showing that UCLA is working across the entire path from molecule to mouse to mechanism to movement to medicine.

Levenson-Cano on Esoteric Thoughts on Diagnostics Value (Digital Pathology)

 From linked in

https://www.linkedin.com/feed/update/urn:li:activity:7449321437858983936/

https://media.licdn.com/dms/document/media/v2/D4E1FAQF1ZruJd48XZA/feedshare-document-pdf-analyzed/B4EZ2CmMPTGQAY-/0/1776012544444

TL;DR: this is not a valuation memo in any normal business sense. It is a philosophical cautionary essay about AI in diagnostics. Their basic point is: AI can become very good at the “game” of internal pattern recognition while still missing the real-world patient, context, accountability, and consequences.

In plain English, they are saying: don’t confuse a beautiful, high-performing AI system with actual clinical wisdom. They use Hesse to symbolize an elegant closed intellectual world detached from life, Gödel to argue that a complex system cannot fully validate itself from inside its own rules, and Wagner to warn that seamless integration can hide what is missing. Then they apply that to pathology: the slide is not the tumor, and the tumor is not the patient. So even a very impressive AI can be blind to the larger clinical reality.

Their practical message is pretty simple underneath the opera-and-philosophy packaging: medical AI needs external governance, real-world validation, visible responsibility, and explicit operating limits. They worry about feedback loops where AI-trained-on-AI drifts away from biology, about opaque tech companies/labs, and about diffused accountability when no one can say who actually owned a bad decision.

So, what are these guys thinking? Basically:
They are thinking “AI in pathology is powerful, but don’t let the elegance of the system hypnotize you.” This is much more a warning essay / governance manifesto than a practical commercial, reimbursement, or valuation analysis.

My blunt gloss: they’re saying the digital pathology / AI crowd risks building a very smart Castalia—brilliant at abstractions, weaker at remembering the patient in the bed.

See also PHILLIPS 2026

https://www.discoveriesinhealthpolicy.com/2026/04/phillips-et-al-in-science-diagnostics.html

See also CLAEYS PRINZI TIMBROOK 2026

https://www.discoveriesinhealthpolicy.com/2026/03/horizons-in-diagnostics-value-case.html

Los Angeles: What Can the 1920s Tell Us About the 2020's?

“Los Angeles: What Can the 1920s Tell Us About the 2020s?”

Los Angeles feels unusually haunted by its own past because the city still wears, in stone and stucco, the ambitions of the 1920s. Walk through Hollywood, downtown, Koreatown, or the old boulevard corridors.  You keep meeting the 1920s decade again and again: movie palaces, courtyard apartments, ornate office blocks, grand churches, towers, stairways, and façades built with the confidence of a city that believed its future would be bigger than its present. 

That impression is not merely sentimental. A remarkable share of central Los Angeles’s visual identity really does come from the great metropolitan surge of the 1920s, when population growth, speculative real estate, automobile culture, oil wealth, and the rise of the film industry all reinforced one another. (Encyclopedia Britannica)

So what can the 1920s tell us about the 2020s? First, they remind us that Los Angeles has always been a boom-built city. Its character was shaped not by slow continuity but by bursts of reinvention. The 1920s were one of those rare moments when nearly everything seemed to expand at once: neighborhoods, studios, churches, institutions, commercial corridors, and civic self-belief. Buildings from that era still feel charged with momentum because they were erected by people who thought they were standing at the start of something immense. (Encyclopedia Britannica)

Second, the 1920s suggest that Los Angeles thrives when it possesses a convincing story about its own future. That is precisely what feels unstable in the 2020s. The film economy has weakened, with FilmLA reporting a 22.4% decline in on-location filming in the first quarter of 2025. Office real estate has remained under severe pressure; Cushman & Wakefield reported overall Los Angeles office vacancy at 24.1% in Q2 2025. And the mood downtown is troubled enough that the Los Angeles Times recently summarized it in plain words: “DTLA is hurting.” (FilmLA)  From vacant offices to vacant restaurants to crime, it seems dark.

The deeper lesson, then, is not that the 1920s were simply glorious while the 2020s are simply grim. It is that Los Angeles has always depended on imagination as much as economics. The city becomes most itself when it believes in its next act. The poignant thing about Los Angeles now is that it still looks like a boomtown of destiny, while often feeling like a metropolis in retrenchment. The arches, towers, and old façades of the 1920s are more than relics. They are reminders that this city was built before, and at high speed, by people who were certain the future was arriving here first. The question for the 2020s is whether and how Los Angeles can recover that confidence in a new form.

AI Dialog; Comparing DUEL (1969) and THE FALL (2022)

THIS IS MID-DIALOG, WHERE I RAISED THE COMPARISON OF "DUEL" AND "FALL".   For the original start of dialog, see futher below.

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FALL, about two women trapped on a high desert radio tower, seems to remind me of the Steven Spielberg movie called DUEL because it is a paradoxical mix of claustrophobic and wide open. 

The truck movie takes place in a wide open desert, yet it feels claustrophobic because much of it is filmed inside the car which is very small and always has the truck on its tail in the rearview mirror. So it is a mix of helicopter shots of wide open desert and great claustrophobic terror. Similarly, in the movie FALL, they are high in space and surrounded by nothing but air and sky, and it feels claustrophobic because this is all filmed within a few feet of the actors faces and bodies on the tiny platform.  Contrast and compare.

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Yes — that is a very sharp comparison, and I think you’ve put your finger on the key formal paradox in both films.

Both Duel and Fall are built on a tension between openness of setting and imprisonment of experience. Duel takes place on open roads in broad daylight across empty desert and scrubland, yet Spielberg repeatedly traps us inside David Mann’s subjective space: the car interior, the windshield frame, the side mirror, the rearview mirror, the speedometer, the panicked glances. Critics and commentators have long noted how much of the film’s suspense comes from POV driving shots and from the truck’s recurring presence in mirrors rather than from any ornate plotting. (citizencant.com)

Fall uses the same contradiction in a vertical form. The women are surrounded by immense empty sky, but that openness does not feel freeing; it feels like the absence of all escape routes. Reviews emphasized exactly this effect: wide and overhead shots establish terrifying exposure, while the film then cuts back into the cramped bodily space of a tiny platform, keeping the suspense close to faces, hands, feet, and the corroded metal around them. (Roger Ebert)

So the two films share a structural trick:

maximum physical openness, maximum psychological enclosure. (citizencant.com)

But they achieve it in slightly different ways.

In Duel, the claustrophobia is created by pursuit. The road is open, but David Mann is never free because the truck occupies his mental field. Even when it is not literally bumper-to-bumper, it invades the frame as menace: in the mirror, in the sound design, in his anticipatory panic. And because Spielberg keeps the truck driver largely unseen, the threat becomes strangely abstract and omnipresent, almost less a person than a system or force. That helps make the desert feel not liberating but exposed and inescapable. (Hagerty UK)

In Fall, the claustrophobia is created not by pursuit but by immobility. Nobody is chasing them. The prison is the platform itself. The enormous surrounding space makes their confinement feel harsher, because every inch beyond the platform is unusable void. In Duel, the hero can keep moving but cannot shake the terror. In Fall, the heroine cannot move at all except within a space of a few feet. That is why the film feels both aerial and suffocating. (Roger Ebert)

There is also a nice contrast in how the films use scale.

In Duel, the truck is huge relative to the car. The visual drama is based on disproportion: one small vulnerable machine harried by one enormous brutal machine. The landscape stays horizontal and the danger keeps arriving from behind or alongside. In Fall, the human body is tiny relative to the tower and the sky. The scale shock is not lateral but vertical. Instead of being dwarfed by another vehicle, the characters are dwarfed by altitude itself. (citizencant.com)

The result is that Duel is about pressure, while Fall is about exposure.

• Duel: compression, pursuit, tailgating, mechanical aggression. (citizencant.com)

• Fall: precariousness, vertigo, thirst, bodily vulnerability, dead air around the body. (Roger Ebert)

Another difference is in the emotional texture. Duel is paranoid. The world feels irrational because the attack has no clear motive. Fall is more survivalist and corporeal. Its fear is less “Why is this happening to me?” and more “How long can the body endure this?” That is why Duel feels like a nightmare of modern mobility, whereas Fall feels like an ordeal movie with horror mechanics. (Senses of Cinema)

But your larger point holds beautifully: both films understand that cinematic claustrophobia does not require walls. In fact, sometimes the absence of walls is worse. A tiny car in a huge desert and a tiny platform in a huge sky both become traps because the camera teaches us to feel the characters’ usable world shrinking to almost nothing. (citizencant.com)

So I’d put it this way:

Duel is claustrophobia inside motion.
Fall is claustrophobia inside exposure.

And both rely on the same cinematic paradox: the more open the world becomes, the more imprisoned the protagonist can feel.

If you like, I can also compare Fall to Open Water, which uses almost the exact same formal paradox, but with the sea instead of the sky.

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ORIGINAL START HERE:

 There was an Indie horror movie a year or two ago about two people, I want to say two girls, who climb a very high tower, several hundred feet high, and then the ladder breaks, and they are trapped up there, and they have no food or water and their cell phones die. If I recall, one girl is rescued at the end.

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You’re almost certainly thinking of Fall (2022).

It’s about two young women who climb an abandoned 2,000-foot TV/radio tower, the ladder gives way, and they end up stranded at the top with almost no supplies. By the end, one survives and is rescued. (Wikipedia)

A few details in your memory line up especially well:

• two women

• very high tower

• ladder breaks

• trapped without food/water

• phone problems

• one rescued at the end (Wikipedia)

One small correction: it was 2022, so about 3–4 years ago, not just one or two. (Wikipedia)

The tower in the film was inspired by the real Walnut Grove broadcast tower in California. (Wikipedia)

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Not as an actual event.

The movie’s story is fictional, but it was visually inspired by a real broadcast tower: the KXTV/KOVR tower in Walnut Grove, California, which is about 2,049 feet tall. Director Scott Mann has said the film’s fictional tower was inspired by that real structure.

So the split is:

Real tower: yes.
Real incident of those two women getting stranded there: no, not as the basis of the film.

And one small wrinkle: in the movie, the tower is presented as an abandoned “B67” tower, but the real Walnut Grove tower is an actual communications structure, not that fictional backstory.

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 How does the movie end? Spoilers are OK. I think one of the girls actually dies in the middle of the movie? But that is not revealed. I understand the film was very challenging because they did not film 1000 feet high but they did film at the top of a fairly high reel tower constructed for the movie.

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Yes — your memory is basically right.

How it ends:
Hunter appears to survive for much of the second half and keeps talking with Becky, helping her think through survival options. But near the end Becky realizes that Hunter actually died earlier when she fell onto the satellite dish and then down the tower. Becky has been hallucinating her presence because of dehydration, exhaustion, and trauma. (Wikipedia)

After that reveal, Becky uses Hunter’s body in a grim but practical way: she places her phone in Hunter’s shoe/body so it can be dropped farther down, where it finally sends a text and photo message to her father. Rescue then comes, and Becky survives. (EW.com)

On the production side, your understanding is also right. The filmmakers did not shoot at 1,000 or 2,000 feet. Director Scott Mann said they built the top section of the tower on top of a mountain in the Mojave Desert, so the actors appeared to be thousands of feet up while actually being about 100 feet off the ground. They chose that instead of relying mainly on green screen. (Wikipedia)

So the movie’s trick was:

real height enough to terrify the actors, plus mountain elevation to fake extreme altitude. (MovieWeb)

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I assume the actress had clips for safety, which were taken out in post reduction

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Yes — almost certainly. They would have been using safety harnesses, rigging, and fall-protection gear, with at least some of it hidden by framing and some of it removed digitally in post. Director Scott Mann said the film was shot largely for real on a tower-top set about 100 feet above the ground, but he also explicitly mentioned “wire paint outs” in postproduction. (Post Magazine)

So the usual formula seems to have been:

real physical height to create genuine fear and body language,
plus hidden safety clips/wires,
plus digital cleanup afterward. (Post Magazine)

That is also why the movie feels so unnerving. It was not just actors on a green screen stage. They were genuinely up on a high practical set, but not recklessly unprotected. Scott Mann described the shoot as mostly practical, with the straight-down shots extended digitally and with some wire removal in post. (Post Magazine)

So your phrase “taken out in post reduction” is basically right — in film language, painted out in post.

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How was the movie received critically?

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It was received pretty well, though not reverently.

Critics mostly treated Fall as a lean, effective B-thriller: a film with a somewhat absurd premise that nonetheless delivered real tension and vertigo. On Rotten Tomatoes, the critics’ consensus was that it is “fundamentally absurd” but also a “sustained adrenaline rush,” which captures the overall tone of the response nicely. (Rotten Tomatoes)

The review scores landed in the solid-to-good range rather than the “great film” range. Rotten Tomatoes listed it at 79% with critics, while Metacritic had it at 62, which is generally interpreted as mixed to positive reviews. (Rotten Tomatoes)

The split in opinion was fairly clear. Supportive critics praised its precision, nerve, and sheer suspense mechanics. The Guardian, for example, called it a “wildly effective survival thriller” and admired how much excitement it wrung from such a stripped-down premise. (The Guardian)

More skeptical critics tended to say: good concept, shakier execution. RogerEbert.com called it a “misfire,” arguing that the premise only takes the movie so far and criticizing elements of the acting, editing, and technical execution. (Roger Ebert)

So the fairest summary is:

Critically, it was respected as a tense, clever, efficiently made thriller, but not generally regarded as a major film. The praise was mostly for physical suspense and nerve, while the criticism centered on implausibility, repetition, and uneven execution. (Rotten Tomatoes)

That actually fits the kind of movie it is: a picture people admire for making their palms sweat, even when they roll their eyes a little.

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