Sunday, November 23, 2025
Neurelis apology
Saturday, November 22, 2025
Do classic psychedelics increase the risk of seizures?
Soto-Angona Ó, Fortea A, Fortea L, Martínez-Ramírez M, Santamarina E, López FJG, Knudsen GM, Ona G. Do classic psychedelics increase the risk of seizures? A scoping review. Eur Neuropsychopharmacol. 2024 Aug;85:35-42. doi: 10.1016/j.euroneuro.2024.05.002. Epub 2024 Jun 24. PMID: 38917636.
Abstract
Seizures are a concerning adverse event frequently associated with the use of psychedelics, and hence, studies involving these substances tend to exclude patients with past history of epilepsy. This is especially relevant because epileptic seizures are markedly increased in the population suffering from mental disorders, and psychedelic assisted therapy is being researched as a promising treatment for several of them. To determine the extent of the current literature on the relationship between classic psychedelics and seizures, a scoping review was performed using the PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews). The search was conducted in PubMed, Web of Science, Google scholar, LILACS and Scielo, and both animal and human models were included. A total of 16 publications on humans, and 11 on animals, were found. The results are heterogeneous, but globally suggest that psychedelics may not increase the risk of seizures in healthy individuals or animals in the absence of other drugs. However, concomitant use of other substances or drugs, such as kambo or lithium, could increase the risk of seizures. Additionally, these conclusions are drawn from data lacking sufficient external validity, so they should be interpreted with caution. Future paths for research and a summary on possible neurobiological underpinnings that might clarify the relationship between classical psychedelics and seizures are also provided.
Thursday, November 20, 2025
Autoimmune autonomic ganglionopathy
Annaliese Holland, 25, said she has been ill since she was a child, enduring repeated hospital stays as doctors tried to diagnose an illness that caused chronic pain, nausea and vomiting — and forced her to depend on IV feeding for the past decade, she told News.com.au.
She was diagnosed with autoimmune autonomic ganglionopathy, a rare autoimmune disease in which the body attacks the autonomic ganglia, the nerves responsible for controlling involuntary bodily functions, according to the Cleveland Clinic.
Years before her diagnosis, Holland’s bowels acted as if they were blocked, despite there actually being nothing stopping them.
Feeding tubes proved ineffective as she continued vomiting, and once doctors realized her stomach wasn’t emptying, they placed her on total parenteral nutrition, which supplies nutrients through an IV to bypass digestion.
“Because of the line straight into your bloodstream, if you get an infection, it turns to sepsis really quickly, which is very, very dangerous,” Holland said, adding that she has survived sepsis — a life-threatening reaction in which the body’s response to an infection damages its own tissues and organs — 25 times.
After doctors spent the majority of her young life trying to pinpoint what illness had been plaguing her, it wouldn’t be until Holland turned 18 and was transferred to an adult hospital that she would get an answer.
Holland said she had been told her condition was terminal when she turned 22.
Holland’s medications have weakened her bones to the point of severe osteoporosis, leaving her in constant pain and resulting in four spinal fractures, a fractured sternum, and nearly catastrophic pressure on her heart and lungs.
“I was so miserable,” Holland said. “You can’t change it so you have to just deal with it really. Even though there’s beautiful moments in my days, they are exhausting and long. I’m in chronic debilitating pain.”
Her illness has left her watching life race by from a hospital room, where she spent her 18th and 21st birthdays, as her friends now marry and start families.
“Everyone’s life is moving and I’m just stuck. I’m not living. I’m surviving every day, which is tough,” she said, noting that her disease feels like “walking on a field of landmines.”
“No man wants to date someone dying, I get it.”
Knowing that her life will end, the 25-year-old said she has decided to “die on my own terms” with voluntary assisted dying (VAD) — a legal option in Australia that provides terminally ill patients with self-administered life-ending medication.
She has watched life race ahead from her hospital room — where she spent her 18th and 21st birthdays — while her friends move on to marriages and families.
“Life for me now is getting up each day doing what I need to do medically, taking the painkillers, trying to get through the day, just to go to bed and do it all again,” she said.
“I have the most incredible team of doctors and nurses who have watched what I have been through and I told them I don’t want this anymore.”
While Holland appears at peace with the decision, her parents and sister are shattered by the idea.
“I remember talking to my dad in the kitchen one night and I said, ‘Dad, I’ve had enough.’ And he went, ‘So you’re giving up?’” she said.
She said the turning point for her father, Patrick, came when she was revived by doctors in the hospital and pleaded, “Dad, please let me go. I won’t hate you if you do.”
“I said, ‘If this happens again, I don’t want anything. And please know that in my heart, you letting me go and saying no to treatment … I’m happy with and that’s what I want,’” Holland said, fighting back tears.
“He turned to me and goes, ‘I don’t know how you do it and I totally understand that you’ve had enough.’”
Holland’s mom, Armanda, said she still hopes for a miracle, though she “realistically understands the challenges” her daughter faces.
Knowing that her life will end, the 25-year-old said she has decided to “die on my own terms” with voluntary assisted dying — a legal option in Australia that provides terminally ill patients with self-administered life-ending medication.
Following a three-week evaluation process, Holland was approved for VAD.
“I think it’s so weird to be happy, but I was so happy when I found out I was approved, I was crying,” she recalled.
“It’s hard because for me I am in pain and then I am at peace, but then I put the pain onto my family. You have this battle in your head of not wanting to hurt them so I will put some thought into how it will happen.”
Holland added that she’s “lucky that I do have this choice.”
“It’s one of the bravest things you could ever do, to say I want VAD. It’s not giving up. You’ve had enough and you fought bloody hard.”
Richard Pollina
https://nypost.com/2025/11/20/world-news/terminally-ill-australian-woman-annaliese-holland-to-die-on-own-terms-after-battling-rare-neurological-disease-her-entire-life/
Wednesday, November 19, 2025
Clinical, radiologic, and pathologic associations of executive dysfunction in children with focal cortical dysplasia–related epilepsy
Abstract
Background and Objective
Executive dysfunction (ExD) is a common comorbidity of focal epilepsy. Focal cortical dysplasia (FCD) is the most common lesional cause of epilepsy in children. We aimed to investigate clinical, etiologic (pathology), and anatomic vs functional network associations with ExD in FCD-related epilepsy. FCD lesion-network interactions may underlie ExD. The primary analysis was to evaluate whether FCD colocalization to frontoparietal control network or attention networks is associated with ExD. We also evaluated whether FCD type I pathology is associated with ExD because it is reported to be associated with worse intellectual function.
Methods
Patients with FCD were included from retrospective surgical/radiologic databases at Children's National Hospital from January 2000 to January 2022 if they had preoperative neuropsychological testing. FCD colocalization to the Yeo 7-network atlas was determined. Clinical, radiologic, and pathologic factors were evaluated for association with ExD. The primary outcome measure was ExD measured categorically (ExD/Not ExD) and linearly (Behavior Rating Inventory of Executive Function [BRIEF]-Global Executive Composite [GEC] T-score).
Ninety-three patients with FCD (45% female) had preoperative BRIEF-GEC T-scores sampled at 11.4 years (SD 4.5 years). Control network colocalization (odds ratio [OR] 3.6, 95% CI 0.94–13.9, p < 0.05) and FCD type I (OR 4.45, 95% CI 1.39–14.3, p = 0.009) are associated with ExD (BRIEF-GEC T-score ≥65). Control network colocalization is associated with Cognitive Regulation Index (mean difference 8.3, 95% CI 0.7–15.9, p = 0.03) and Plan/Organize subscale (8.4, 95% CI 0.9–16.0, p = 0.028). FCD type I is associated with BRIEF-GEC T-score (8.3, 95% CI 2.3–14.2, p = 0.007), Cognitive Regulation Index (7.1, 95% CI 1.2–13.1, p = 0.019), Working Memory (7.4, 95% CI 1.2–13.6, p = 0.021), Plan/Organize (6.0, 95% CI 0.21–11.8, p = 0.042), Shift (8.1, 95% CI 1.6–14.7, p = 0.015), and Emotional Control (8.5, 95% CI 2.5–14.5, p = 0.006) subscales. These findings were not related to Full Scale IQ. FCD colocalization to attentional network (dorsal or ventral), lobar location, or age seizure onset was not associated with ExD.
Discussion
These data demonstrate the importance of lesion-network interaction in neuropsychological comorbidity (ExD) in focal epilepsy, unrelated to lesion size or lobar location. FCD colocalization to the Frontoparietal Control network is associated with ExD in a heterogeneous cohort of FCD-related epilepsy. A network-level structure-function correlation is suggested as the most affected processes of cognitive regulation (e.g., planning/organization) are domains regulated by this network. This work contributes toward a more unified theory of focal epilepsy, by beginning to explain common neuropsychological deficits seen across the epilepsies by cortical lesion-network interaction and regardless of lobar location.
Laryngeal cleft
“Picture breathing through a milkshake straw, then breathing through a regular straw, then trying to breathe through a coffee straw,” Maria Carlin, 36, recently told The Post of her 4-year-old Jack’s harrowing experience in late July.
“We got to a point where I said to myself, ‘It doesn’t get higher-pitched. … I know what comes next.’ [His breathing] just stopped.”
Carlin, a nurse at North Shore University Hospital, got her stricken son — who was previously undiagnosed — into the car and began driving to the medical facility after he had spent the night crying in agony without “a single symptom of anything.”
Jack suddenly lost all of his air halfway into the 10-minute drive, forcing his mom to make to an impossible choice: pull over to give him CPR or keep rushing to the hospital.
Carlin decided to continue to the ER, knowing immediate resuscitation wouldn’t be enough, given Jack would need rapid intubation among other urgent procedures.
“I heard him slump over. I went to look back, and God said, ‘Maria, don’t look back. You made your decision. You’re not going to be able to handle seeing him right now,’ ” she recalled, fighting back tears.
“Knowing that you have a child in the back of your car who’s not breathing and needs CPR and not doing that for them — I don’t wish that scenario on my worst enemy.”
Carlin made the critical decision to drive Jack to the hospital instead of stopping to give him CPR.
Carlin blared her car horn as she pulled up the car to the doors of ER, and a team of doctors and nurses flew into action over Jack, who was now in cardiac arrest and without a heartbeat.
“I just saw this lifeless kid who had no pulse, who looked blue,” said emergency-room Dr. Jennifer Gibb, who rushed to Jack after hearing Carlin “screaming.”
“I didn’t know she was a nurse at the time,” Gibb said of Carlin.
“I heard her saying, ‘Come on, Jack,’ and that’s my son’s name. It sends chills through your spine when you’re helping this little child that could be your own,” said Gibb of her own 11-year-old son.
Jack’s pulse returned after the doctors and nurses worked on him for almost 10 minutes.
“I can’t even explain what that feeling is like when you know that your child’s heart is beating again,” Carlin said.
Jack was transferred to Cohen Children’s Medical Center a few hours later.
“I’ve been working here for 13 years, and I really only had a pediatric arrest like that, maybe about five times,” Gibb said.
Further examinations showed he had a laryngeal cleft, which impacts between 10,000 and 20,000 annual births, according to Northwell.
“It’s an abnormal opening in the back of the voice box that separates the voice box from the esophagus,” said Dr. Lee Smith, Cohen’s chief of pediatric otolaryngology.
Mucus or fluids can block airflow as a result of the “extremely uncommon” occurrence.
The boy’s dire situation was even more incredibly unique, according to Smith, who later performed his corrective surgery with no complications.
“I’ve never seen that before. … This was an extremely unusual and severe presentation,” Smith said of the boy losing lethal amounts of air.
“The survival rate of a child going into cardiac arrest outside of a hospital is terrifyingly low,” Carlin said.
“After everything happened, I turned to my husband, and I was just like, ‘We’re going to Disney World. This child is going to experience Disney World.’ “8Jack told The Post he enjoyed his vacation and is happy in pre-K.
“I really liked the Slinky ride,” Jack told The Post.
“And I love being in school.”
Alex Mitchell
https://nypost.com/2025/11/19/us-news/li-moms-impossible-decision-saves-lifeless-child-and-reveals-exceptionally-rare-condition/
Monday, November 17, 2025
Skeletal muscle MRI patterns in female dystrophinopathy carriers
Abstract
Background and objectives: Dystrophinopathies are X-linked recessive diseases caused by pathogenic variants in the Duchenne muscular dystrophy (DMD) gene. Some women carrying a single DMD pathogenic variant manifest variable levels of symptomatology. Those who manifest severe and early-onset symptoms are considered to be affected by dystrophinopathy rather than carriers. The aim of this study was to characterize and compare muscle structure between female DMD carriers who were asymptomatic at the time of the study and female control participants using whole-body MRI (WB-MRI) and correlate the findings with clinical and genetic data.
Methods: We conducted a cross-sectional observational study comparing a group of female carriers of DMD pathogenic variants and a group of healthy noncarrier controls. The first group included obligate and genetically confirmed DMD female carriers, not classified as having dystrophinopathy. Women in the healthy group had no family history of DMD or other muscular dystrophies. All individuals underwent WB-MRI, which was evaluated using qualitative grading scales to assess muscle edema, trophism, and fatty infiltration. Neurologic examinations, serum creatine kinase measurement, DMD genetic screening, and X-chromosome inactivation studies were performed on the DMD carriers.
Results: The study included 29 DMD female carriers and 30 healthy noncarrier controls. All DMD carriers showed signs of muscle involvement on MRI, revealing a larger proportion of skeletal muscle involvement in carriers than in controls (85% vs 27% of 48 examined muscles/group of muscles, p < 0.001). Edema, fatty infiltration, and atrophy were more common in DMD carriers (62.5% vs 8%; 81% vs 35%; and 81% vs 25%, respectively, all p < 0.001), particularly in muscles of the calves, thighs, and pelvic region. The most frequently affected muscles were gastrocnemius, gluteus maximus, and soleus. No correlations were found between the MRI results and the clinical and genetic data.
Discussion: Our findings indicate that DMD female carriers who are asymptomatic at the time of our study may be at risk of developing muscle symptoms at a future time. Multidisciplinary surveillance of DMD female carriers will facilitate early detection and management of complications.
Friday, November 14, 2025
Brain-responsive neurostimulation for epilepsy
Abstract
Objective: To prospectively evaluate safety and efficacy of brain-responsive neurostimulation in adults with medically intractable focal onset seizures (FOS) over 9 years.
Methods: Adults treated with brain-responsive neurostimulation in 2-year feasibility or randomized controlled trials were enrolled in a long-term prospective open label trial (LTT) to assess safety, efficacy, and quality of life (QOL) over an additional 7 years. Safety was assessed as adverse events (AEs), efficacy as median percent change in seizure frequency and responder rate, and QOL with the Quality of Life in Epilepsy (QOLIE-89) inventory.
Results: Of 256 patients treated in the initial trials, 230 participated in the LTT. At 9 years, the median percent reduction in seizure frequency was 75% (p < 0.0001, Wilcoxon signed rank), responder rate was 73%, and 35% had a ≥90% reduction in seizure frequency. We found that 18.4% (47 of 256) experienced ≥1 year of seizure freedom, with 62% (29 of 47) seizure-free at the last follow-up and an average seizure-free period of 3.2 years (range 1.04-9.6 years). Overall QOL and epilepsy-targeted and cognitive domains of QOLIE-89 remained significantly improved (p < 0.05). There were no serious AEs related to stimulation, and the sudden unexplained death in epilepsy (SUDEP) rate was significantly lower than predefined comparators (p < 0.05, 1-tailed χ2).
Conclusions: Adjunctive brain-responsive neurostimulation provides significant and sustained reductions in the frequency of FOS with improved QOL. Stimulation was well tolerated; implantation-related AEs were typical of other neurostimulation devices; and SUDEP rates were low.
Clinicaltrialsgov identifier: NCT00572195.
Classification of evidence: This study provides Class IV evidence that brain-responsive neurostimulation significantly reduces focal seizures with acceptable safety over 9 years.
Geller EB, Skarpaas TL, Gross RE, Goodman RR, Barkley GL, Bazil CW, Berg MJ, Bergey GK, Cash SS, Cole AJ, Duckrow RB, Edwards JC, Eisenschenk S, Fessler J, Fountain NB, Goldman AM, Gwinn RP, Heck C, Herekar A, Hirsch LJ, Jobst BC, King-Stephens D, Labar DR, Leiphart JW, Marsh WR, Meador KJ, Mizrahi EM, Murro AM, Nair DR, Noe KH, Park YD, Rutecki PA, Salanova V, Sheth RD, Shields DC, Skidmore C, Smith MC, Spencer DC, Srinivasan S, Tatum W, Van Ness PC, Vossler DG, Wharen RE Jr, Worrell GA, Yoshor D, Zimmerman RS, Cicora K, Sun FT, Morrell MJ. Brain-responsive neurostimulation in patients with medically intractable mesial temporal lobe epilepsy. Epilepsia. 2017 Jun;58(6):994-1004. doi: 10.1111/epi.13740. Epub 2017 Apr 11. PMID: 28398014.
Abstract
Objective: Evaluate the seizure-reduction response and safety of mesial temporal lobe (MTL) brain-responsive stimulation in adults with medically intractable partial-onset seizures of mesial temporal lobe origin.
Methods: Subjects with mesial temporal lobe epilepsy (MTLE) were identified from prospective clinical trials of a brain-responsive neurostimulator (RNS System, NeuroPace). The seizure reduction over years 2-6 postimplantation was calculated by assessing the seizure frequency compared to a preimplantation baseline. Safety was assessed based on reported adverse events.
Results: There were 111 subjects with MTLE; 72% of subjects had bilateral MTL onsets and 28% had unilateral onsets. Subjects had one to four leads placed; only two leads could be connected to the device. Seventy-six subjects had depth leads only, 29 had both depth and strip leads, and 6 had only strip leads. The mean follow-up was 6.1 ± (standard deviation) 2.2 years. The median percent seizure reduction was 70% (last observation carried forward). Twenty-nine percent of subjects experienced at least one seizure-free period of 6 months or longer, and 15% experienced at least one seizure-free period of 1 year or longer. There was no difference in seizure reduction in subjects with and without mesial temporal sclerosis (MTS), bilateral MTL onsets, prior resection, prior intracranial monitoring, and prior vagus nerve stimulation. In addition, seizure reduction was not dependent on the location of depth leads relative to the hippocampus. The most frequent serious device-related adverse event was soft tissue implant-site infection (overall rate, including events categorized as device-related, uncertain, or not device-related: 0.03 per implant year, which is not greater than with other neurostimulation devices).
Significance: Brain-responsive stimulation represents a safe and effective treatment option for patients with medically intractable epilepsy, including patients with unilateral or bilateral MTLE who are not candidates for temporal lobectomy or who have failed a prior MTL resection.
Jobst BC, Kapur R, Barkley GL, Bazil CW, Berg MJ, Bergey GK, Boggs JG, Cash SS, Cole AJ, Duchowny MS, Duckrow RB, Edwards JC, Eisenschenk S, Fessler AJ, Fountain NB, Geller EB, Goldman AM, Goodman RR, Gross RE, Gwinn RP, Heck C, Herekar AA, Hirsch LJ, King-Stephens D, Labar DR, Marsh WR, Meador KJ, Miller I, Mizrahi EM, Murro AM, Nair DR, Noe KH, Olejniczak PW, Park YD, Rutecki P, Salanova V, Sheth RD, Skidmore C, Smith MC, Spencer DC, Srinivasan S, Tatum W, Van Ness P, Vossler DG, Wharen RE Jr, Worrell GA, Yoshor D, Zimmerman RS, Skarpaas TL, Morrell MJ. Brain-responsive neurostimulation in patients with medically intractable seizures arising from eloquent and other neocortical areas. Epilepsia. 2017 Jun;58(6):1005-1014. doi: 10.1111/epi.13739. Epub 2017 Apr 7. PMID: 28387951.
Abstract
Objective: Evaluate the seizure-reduction response and safety of brain-responsive stimulation in adults with medically intractable partial-onset seizures of neocortical origin.
Methods: Patients with partial seizures of neocortical origin were identified from prospective clinical trials of a brain-responsive neurostimulator (RNS System, NeuroPace). The seizure reduction over years 2-6 postimplantation was calculated by assessing the seizure frequency compared to a preimplantation baseline. Safety was assessed based on reported adverse events. Additional analyses considered safety and seizure reduction according to lobe and functional area (e.g., eloquent cortex) of seizure onset.
Results: There were 126 patients with seizures of neocortical onset. The average follow-up was 6.1 implant years. The median percent seizure reduction was 70% in patients with frontal and parietal seizure onsets, 58% in those with temporal neocortical onsets, and 51% in those with multilobar onsets (last observation carried forward [LOCF] analysis). Twenty-six percent of patients experienced at least one seizure-free period of 6 months or longer and 14% experienced at least one seizure-free period of 1 year or longer. Patients with lesions on magnetic resonance imaging (MRI; 77% reduction, LOCF) and those with normal MRI findings (45% reduction, LOCF) benefitted, although the treatment response was more robust in patients with an MRI lesion (p = 0.02, generalized estimating equation [GEE]). There were no differences in the seizure reduction in patients with and without prior epilepsy surgery or vagus nerve stimulation. Stimulation parameters used for treatment did not cause acute or chronic neurologic deficits, even in eloquent cortical areas. The rates of infection (0.017 per patient implant year) and perioperative hemorrhage (0.8%) were not greater than with other neurostimulation devices.
Significance: Brain-responsive stimulation represents a safe and effective treatment option for patients with medically intractable epilepsy, including adults with seizures of neocortical onset, and those with onsets from eloquent cortex.
Thursday, November 13, 2025
Decimal point error in a potassium prescription
A 2-year-old boy died in a Florida hospital after a doctor negligently deleted a decimal point in his prescription, resulting in the underweight toddler receiving 10 times the dosage of medicine he should have, a lawsuit alleges.
De’Markus Page “tragically overdosed with potassium” on March 3, 2024, causing him to suffer a massive brain injury and forcing him to spend the next two weeks enduring “a horrific and protracted hospital course” on a ventilator before finally being taken off life support, according to a lawsuit filed by his mother last week.
Mom Dominique Page is suing University of Florida Health and its Shands Teaching Hospital and Clinics, as well as the medical staff that she claims “fumbled” his treatment, including taking 20 minutes to intubate him after he went into cardiac arrest, the Alachua County Circuit Court lawsuit alleges.
De’Markus — who “was suspected of having some level of autism” and was a picky eater — first landed in AdventHealth Ocala Hospital on March 1, 2024, with a virus and dangerously low levels of potassium, Law & Crime first reported, citing the suit.
He was given intravenous fluids to help with his low electrolyte levels and the next morning transferred to Shands Teaching Hospital and Clinics in Gainsville, Fla., “in order to receive the higher level of care he required,” the suit claims.
Shands medical staff found De’Markus weighed just 21 pounds — the 30th percentile of weight for his demographic — and he still had low levels of potassium, the court papers explain.
So the boy was given “electrolyte replacement therapy,” but the next day, Dr. Jiabi Chen “unconscionably” ordered that the boy be given “10 times the level ordered the previous day,” which had “been calculated based on his size, weight, and that day’s lab results,” the filing alleges.
Chen “errantly” ordered the extremely high dosage, “deleting a critical decimal point in the prior day’s dosage of 1.5 mmol — now ordering the liquid supplement to be given at 15 mmol twice a day,” the suit claims.
This was on top of the two other forms of potassium De’Markus was already receiving through IV and Pedialyte, the filing charges.
No one else on the medical team, or the pharmacists, caught the error “despite a Red Flag warning in the hospital’s pharmacy system that alerted them to the excessive dosage,” the court documents claim.
So the toddler received two of the excessive doses, the last being administered at 8:28 p.m. March 3, 2024, the suit alleges. By 9:02 p.m., he went into cardiac arrest caused by the overdose — or hyperkalemic cardiac arrest, the suit alleges.
De’Markus Page was brought to the University of Florida Health, Shands Children Hospital, where medical staff botched his treatment, according to a suit.
The staff bungled the response and carried out “2 to 3 botched attempts” to intubate De’Markus, the court documents claim. And “there was at least twenty minutes that had passed since the Code [Blue] was called, during which time he remained severely deprived of the oxygen necessary to sustain life,” the suit alleges.
De’Markus’ heart eventually spontaneously came back, “but the anoxic damage already done to his brain and other vital organs was catastrophic,” the suit says.
When his blood was drawn, they found elevated potassium and phosphate, the filing claims.
De’Markus was kept alive for the next two weeks while enduring seizures and battling “myriad of ICU-related complications” before he was taken off life support on March 18, 2024, the filing charges.
Dominique, of Marion County, Fla., is suing Shands and University of Florida for at least $50,000 under wrongful death claims and related claims for the pain her son suffered and for her loss of “companionship of her minor child and for mental pain and suffering” she endured.
The Page family lawyer, Jordan Dulcie, called the hospital and its doctors’ actions “grossly negligent” and said they “failed the basic standards of medical care.”
“No parent should have to lose a child like this,” the lawyer continued. “What the family has endured is unimaginable and the worst part is that it was entirely preventable.”
The lawyer said he hopes to bring the case to trial to prevent another family from having to go through what Dominique went through.
The hospital declined to comment on the case but said: “UF Health is committed to protecting the privacy of all patients and their families and follows all state and federal HIPAA regulations. We cannot release information on patients or possible patients and their treatment without consent.”
Chen didn’t immediately return a request for comment Wednesday.
Priscilla DeGregory
https://nypost.com/2025/11/12/us-news/florida-2-year-old-tragically-died-of-potassium-overdose-after-tot-got-10-times-correct-prescription-suit/
SUDEP in children
Abstract
Objective: This study was undertaken to understand the circumstances surrounding pediatric sudden unexpected death in epilepsy (SUDEP) and identify clinical factors that may be associated with SUDEP in childhood. Methods: A retrospective case series was conducted. Pediatric SUDEP cases were collected across Canada from the Ontario Forensic Pathology Service, Canadian Pediatric Surveillance Program, and Canadian Pediatric Epilepsy Network. Demographics, epilepsy history, comorbidities, and circumstances surrounding death were analyzed. Results: Forty-nine children with pediatric SUDEP were analyzed; 25 (51%) were females, and the median age at death was 8 years. Six children (12%) were <2 years of age at the time of death. Information on seizure types 6 months before death was known in 35 children. Twenty-two had tonic–clonic seizures within the last 6 months prior to death (63%). Seven children (18%) had no tonic–clonic seizures in their lifetime. Two thirds of children were treated with ≥2 antiseizure medications. Genetic etiologies were most common (55%). Data on global developmental delay (GDD) was known in 46 children: 12 children (26%) had no impairment, and 34 were globally delayed (74%). Children with GDD had earlier age at seizure onset (P < .001); however, epilepsy duration was similar to those without GDD (P = .170). Similar to adult cohorts, death was often unwitnessed (n = 41/46, 89%). Information on recent infection before death was known in 37 children. Seventeen children (46%) had a recent infection. Significance: Our study represents the largest pediatric SUDEP case series to date. SUDEP occurred in children of all ages, including infants, with a spectrum of epilepsies with and without neurodevelopmental impairment. The circumstances around death (ie, timing of death, witnessed/unwitnessed) were similar to previous SUDEP cohorts. A recent infection was often observed, which could decrease seizure threshold and trigger a terminal seizure and may suggest that times of increased seizure risk could warrant heightened surveillance for SUDEP. However, further research is needed to determine the significance of this finding.
Joshi C. In the Quest for Answers: Exploring Circumstances Around Pediatric SUDEP. Epilepsy Currents. 2025;0(0). doi:10.1177/15357597251395592 (commentary on Whitney, et al.)
The American Epilepsy Society and American Academy of Neurology recommend discussing Sudden Unexpected Death in Epilepsy (SUDEP) with every patient as soon as possible—at or after the initial visit—as a best practice recommendation. However, most child neurologists do not follow this practice despite the fact that the risk of SUDEP in pediatric patients is no different than the adult population at approximately 1.2 per 1000 person-years. This deviation from best practice is mostly attributed to lack of sufficient knowledge and lack of a feeling of ethical and moral obligation to be discussing SUDEP with families.
While most epileptologists at tertiary care centers have either had experience with SUDEP or are knowledgeable about it, let us review what is already known about SUDEP:
Childhood Epilepsies are Different From Adult Epilepsies but the Risk of SUDEP is Similar! What are the Specific Risk Factors and How Does Each Increase Risk for SUDEP?
Previous small case series had identified SUDEP risk factors including young age at epilepsy diagnosis, long duration of epilepsy, focal epilepsy, intellectual disability as examples. Subsequently, a systematic review published by the American Academy of Neurology in 2017 clarified risk factors. While high frequency of generalized tonic-clonic seizures (GTC) was the only risk factor identified with a high level of confidence; lack of nighttime supervision and absence of nocturnal listening device were identified risk factors with moderate confidence. In general, methodologic limitations due to small numbers, highly selected populations and differences in definitions of potential risk factors hampered such data pooling. The need for large, high-quality studies to assess risk of SUDEP was unmet till 2020 when Sveinsson et al published their study. These results were obtained from a Swedish population-based case control study of SUDEP-related deaths between July 1, 2006, and December 31, 2011. SUDEP incidence under the age of 16 years was 1.11 per 1000 person-years. Key risk factors included experiencing any GTCs during the preceding year, which contributed to a 27-fold increased risk. Further modeling and logistical regression analysis for the presence of exclusively nocturnal GTCs in the preceding year contributed to a 15-fold increased risk while living alone contributed to a five-fold increased risk. Moreover, the interaction of the combination of living alone and having at least one GTC increased the risk by 67-fold. Previously identified associations of young age at epilepsy onset, longer duration of epilepsy, structural etiology became nonsignificant after controlling for GTC frequency in the above study. While Sveinsson's data identified GTCs as the main culprit, the North American SUDEP Registry data published in 2019 brought attention to the fact that, of 143 patients with known information, 60% had focal epilepsy. Additionally, treatment responsive or benign epilepsy (what would now be classified as self-limited epilepsies) contributed to a sizable minority of SUDEP deaths.
Another systematic analysis of pediatric SUDEP published in 2019 concluded that there is currently insufficient evidence to determine etiology of pediatric SUDEP due to methodological issues of noncomparative studies with a high risk of bias. Moreover, GTCs are not a common feature of pediatric epilepsy—especially in the younger age group. Genetic factors have also been posited as additional risk factors in SUDEP. This hypothesis is supported by the increased incidence of SUDEP in children with epilepsies caused by pathogenic variants in genes including SCN1A, SCN8A, DEPDC5.7
Are Circumstances Around Pediatric SUDEP Different?
This would be a logical question to ask because lack of medication adherence, lack of supervision, living alone, as SUDEP-associated risk factors, are likely less applicable in pediatric epilepsy when compared to adult epilepsy. Authors Whitney and Donner investigated the circumstances surrounding SUDEP in Canadian children using SUDEP-related data from the Ontario forensic pathology service (collected over 3 years between December 2014 and 2017), Canadian pediatric surveillance program (pediatricians were surveyed monthly over 2 years between January 2014 and December 2015) and Canadian pediatric epilepsy network (members completed case report form regarding SUDEP between January 1, 2000 and December 31, 2017). This forms the largest retrospective pediatric case series with 49 definite or probable cases of SUDEP to date.
Key Findings in this Paper Related to Epilepsy
1.
Median age at death was 8 years (range 6 months to 17.9 years)
2.
In the six months prior to death, 63% [22/35] children had either primary generalized or focal to bilateral tonic-clonic seizures.
3.
Seven children [18%] had no documented lifetime history of tonic-clonic seizures.
4.
Three children were seizure-free in the 6 months prior to death [one had juvenile myoclonic epilepsy].
5.
Twenty-seven children [55%] had a genetic or presumed genetic etiology while 12 children [25%] had an unknown etiology.
6.
91% of the children were on antiseizure medications (ASM) at the time of death and only 24% children [5/21] had a history of poor compliance.
7.
Seven children had a dosage reduction [7/34, 47%] or had missed a dose in the 24 h preceding death.
Relevant Medical History
Medical history was extracted from the chart and thus further details regarding severity or classification of comorbidities is not known.
1.
Majority of the children had global developmental delay [46/49, 74%].
2.
Seven children were noted to have a cardiac comorbidity [7/43, 16%].
3.
Nine children had a respiratory comorbidity [9 /36, 25%].
Other Notable Variables
1.
Nine children [9/23, 39%] shared a room with someone.
2.
In seven children [7/17, 41%] regular nocturnal checks were performed and in 2 of the 7 children, listening devices were also used.
3.
93% of the patients were asleep [42/45] and death was unwitnessed in 89% [41/46].
4.
Seventeen children [17/37, 46%] were reported to have recent infection prior to death [“recent” is defined as within the same day or few days—per communication with authors].
Findings in Children <2 years of age
Most patients had global developmental delays, were diagnosed with developmental and epileptic encephalopathy, and were on polytherapy with ASMs at the time of death.
Conclusion and Take-Home Message
Authors who are well-respected in the field have put together the largest case series of pediatric SUDEP. However, this data does not add new knowledge that will help to quantify risk associated with above factors for SUDEP in the next pediatric epilepsy patient that you see. Authors published a retrospective case series built on case report forms submitted across several time spans without a population-based control necessary for comparison or quantification of risk factors associated with pediatric SUDEP.
The circumstances around pediatric SUDEP are not vastly different from those of adult SUDEP in this retrospective sample. One valuable and useful study finding adds justification to the practice of giving patients bridge doses of increased ASM around times of illness/infection—especially in patients with other medical comorbidities. Although granularity regarding significance of medical comorbidities, details regarding infection, type of infection, severity of infection related to baseline infection for that child are lacking in the study, bridge dosing may not be an “overkill.” Close to 50% of those lost to SUDEP in the above case series had a prior infection which in turn could have increased chances of terminal seizures.
By capturing the spectrum of pediatric SUDEP, authors have succeeded in highlighting the shocking reality that no child with epilepsy is risk free when it comes to SUDEP. While much more work is needed to individualize and quantify the risk to the next patient I see in clinic; I must continue to talk about SUDEP to ALL my patients with epilepsy. Without being an alarmist, I must counsel patients that NO seizure is risk-free while trying to reduce the frequency of GTCs as best as I can.
https://journals.sagepub.com/doi/full/10.1177/15357597251395592
Whitney R, Keller A, Li S-A, Datta AN, MacDonald M, Nabavi Nouri M, et al. Circumstances surrounding sudden unexpected death in epilepsy in children: A national case series. Epilepsia. 2025; 66: 1988–2000. https://doi.org/10.1111/epi.18339
Abstract
Objective
This study was undertaken to understand the circumstances surrounding pediatric sudden unexpected death in epilepsy (SUDEP) and identify clinical factors that may be associated with SUDEP in childhood.
Methods
A retrospective case series was conducted. Pediatric SUDEP cases were collected across Canada from the Ontario Forensic Pathology Service, Canadian Pediatric Surveillance Program, and Canadian Pediatric Epilepsy Network. Demographics, epilepsy history, comorbidities, and circumstances surrounding death were analyzed.
Results
Forty-nine children with pediatric SUDEP were analyzed; 25 (51%) were females, and the median age at death was 8 years. Six children (12%) were <2 years of age at the time of death. Information on seizure types 6 months before death was known in 35 children. Twenty-two had tonic–clonic seizures within the last 6 months prior to death (63%). Seven children (18%) had no tonic–clonic seizures in their lifetime. Two thirds of children were treated with ≥2 antiseizure medications. Genetic etiologies were most common (55%). Data on global developmental delay (GDD) was known in 46 children; 12 children (26%) had no impairment, and 34 were globally delayed (74%). Children with GDD had earlier age at seizure onset (p < .001); however, epilepsy duration was similar to those without GDD (p = .170). Similar to adult cohorts, death was often unwitnessed (n = 41/46, 89%). Information on recent infection before death was known in 37 children. Seventeen children (46%) had a recent infection.
Significance
Our study represents the largest pediatric SUDEP case series to date. SUDEP occurred in children of all ages, including infants, with a spectrum of epilepsies with and without neurodevelopmental impairment. The circumstances around death (i.e., timing of death, witnessed/unwitnessed) were similar to previous SUDEP cohorts. A recent infection was often observed, which could decrease seizure threshold and trigger a terminal seizure and may suggest that times of increased seizure risk could warrant heightened surveillance for SUDEP. However, further research is needed to determine the significance of this finding.
Monday, November 10, 2025
Scuba diving and epilepsy
Abstract
Recreational scuba diving is a popular sport, and people with epilepsy often ask physicians whether they may engage in diving. Scuba diving is not, however, without risk for anyone; apart from the risk of drowning, the main physiological problems, caused by exposure to gases at depth, are decompression illness, oxygen toxicity, and nitrogen narcosis. In the United Kingdom, the Sport Diving Medical Committee advises that, to dive, someone with epilepsy must be seizure free and off medication for at least 5 years. The reasons for this are largely theoretical. We review the available evidence in the medical literature and diving websites. The risk of seizures recurring decreases with increasing time in remission, but the risk is never completely abolished. We suggest that people with epilepsy who wish to engage in diving, and the physicians who certify fitness to dive, should be provided with all the available evidence. Those who have been entirely seizure-free on stable antiepileptic drug therapy for at least 4 years, who are not taking sedative antiepileptic drugs and who are able to understand the risks, should then be able to consider diving to shallow depths, provided both they and their diving buddy have fully understood the risks.
Smart D, Lippmann J. Epilepsy, scuba diving and risk assessment. Near misses and the need for ongoing vigilance. Diving Hyperb Med. 2013 Mar;43(1):37-41. PMID: 23508661.
Abstract
There is ongoing debate about the safety of scuba diving for individuals with a history of epilepsy. An in-water seizure is highly likely to be fatal. Recommendations for fitness to dive vary with some regarding epilepsy as an absolute contraindication to diving (South Pacific Underwater Medicine Society) and others permitting diving under strict criteria (United Kingdom Sport Diving Medical Committee) with diving to be postponed for a period of three to five years without seizures. Long-term follow up of people with epilepsy shows that at least one-third will have a recurrence and that the risk remains elevated for many years. We present three cases where individuals with a history of epilepsy (or likely epilepsy) almost fell through the cracks of health risk assessment, two with near-fatal consequences. These cases inform the on-going debate about fitness to dive for those with current or past epilepsy, and highlight the importance of education for doctors, dive professionals and divers about the risks associated with epilepsy and diving.
Google AI
Why scuba diving with epilepsy is dangerous
Seizures underwater are often fatal: A seizure underwater can cause the diver to lose their regulator, leading to drowning.
Triggers in the diving environment: Diving can increase the risk of a seizure due to potential triggers like fatigue, stress, anxiety, sensory deprivation, and nitrogen narcosis.
Medication side effects: Anti-epileptic medications can have sedative effects and may exacerbate nitrogen narcosis or cause it to occur at shallower depths.
Strict conditions for diving
Long seizure-free period: Some authorities may consider allowing a person to dive if they have been seizure-free for at least five years, and are also off all medication.
Medical clearance: It is crucial to consult with a diving doctor and a neurologist to discuss the risks and potential for medical clearance.
Understanding risks: The diver and their buddy must be fully aware of the increased risks involved.
Alternatives to scuba diving
Many other activities are safe and enjoyable for people with epilepsy, as long as precautions are taken and reasonable safety equipment is used.
Examples include biking, contact and non-contact sports, and running.
Leg movement variability and dystonia diagnosis
Now, an interdisciplinary research team led by Bhooma Aravamuthan, MD, DPhil, an assistant professor of neurology at Washington University School of Medicine in St. Louis, has identified an objective way of measuring leg dystonia in children with cerebral palsy. Their method evaluates leg movement variability — specifically, the extent to which a child’s legs adduct, or move toward the center of the body, while they’re sitting down. With this straightforward method, doctors can quickly and accurately determine the severity of dystonia in their patients and tailor treatments to their needs.
In an effort to better understand the causes of dystonia, the researchers then identified in mice the conditions and brain region linked with leg movement variability, suggesting that early medical intervention targeting the relevant brain processes could effectively treat or even prevent this common complication.
“An overarching goal of this work is about standardizing dystonia assessment by quantifying diagnoses that were previously based on doctors’ gut feelings,” said Aravamuthan, who started the project while being mentored in the lab of co-senior author Jordan McCall, PhD, an associate professor of anesthesiology at WashU Medicine. “These results can be immediately put into clinical practice to help guide treatment selection for children with cerebral palsy and ultimately improve patient outcomes.”
Leveraging technology to measure movement
Despite being a common feature of cerebral palsy, dystonia has proven difficult to pin down in earlier research because of its variability of symptoms, which may be subtle and only appear during specific activities or when a child is stressed. Inspired by her work with pediatric neurology patients, Aravamuthan and her collaborators set out to both quantify the clinical presentation of leg dystonia and determine its causal mechanism in the brain, with the goal of making standardized evaluation and treatment available for patients immediately.
Aravamuthan’s study had two main parts. First, a panel of eight pediatric movement disorder specialists practicing at different institutions across the U.S. watched videos of 193 children ages three and up with cerebral palsy performing a seated task with their hands. They found that the variability in the child’s leg movements correlated strongly with the severity of their dystonia as assessed from the videos, suggesting that this variability — which is objectively and quantitatively measurable in an office setting in terms of the angle and position of the child’s legs as they move toward the midline of the body — could be used as a reliable marker of the disorder.
“We were able to establish concrete guidelines that physicians can use today to evaluate dystonia in patients with cerebral palsy more accurately,” said Aravamuthan. “That will make treatment better for our patients as well as support drug development and future research that can rely on this consistent and reproducible assessment method.”
In the second part of the study, Aravamuthan’s team tested whether stimulating specialized brain cells in the region associated with motor control could cause similar leg movement variability in mice as that observed in people. These cells, called striatal cholinergic interneurons (ChIs), play a key role in coordinating muscle movements and ensuring smooth and purposeful actions, making them a promising target for developing treatments for dystonia.
Researchers in Aravamuthan’s lab selectively excited these neurons in mice over 14 days. They observed that mice with chronic ChI excitation displayed increased leg movement variability compared to mice without ChI excitation, mimicking the dystonia seen in people with cerebral palsy. This did not happen with short-term excitation, showing that sustained activity in these neurons is necessary to produce the dystonia. This suggests that drugs that target overactive striatal ChIs could be a promising approach for treating dystonia.
“We know from the clinic that it takes weeks, months or sometimes even years after brain injury for someone to develop dystonia,” Aravamuthan said. “There are medications already in use that focus on reducing excitability of these neurons, but they’re given after dystonia has already been present for a while, which may be why they’re only variably effective. Our work in mice suggests that if you give these medications early and prevent chronic excitation of these neurons, you may prevent dystonia from happening.”
Aravamuthan added that additional experiments and drug trials would be required before such interventions see clinical use.
Shawn Ballard
https://medicine.washu.edu/news/new-method-more-accurately-assesses-movement-disorder-in-children/
Gemperli K, Lu X, Chintalapati K, Rust A, Bajpai R, Suh N, Blackburn J, Gelineau-Morel R, Kruer MC, Mingbunjerdsuk D, O’Malley J, Tochen L, Waugh JL, Wu S, Feyma T, Perlmutter J, Mennerick S, McCall JG, Aravamuthan BR. Chronic striatal cholinergic interneuron excitation causes cerebral palsy-related dystonic behavior in mice. Annals of Neurology. Online July 3, 2025. DOI: https://onlinelibrary.wiley.com/doi/10.1002/ana.27299
Abstract
Objective
Mouse models of genetic dystonias have demonstrated abnormal striatal cholinergic interneuron excitability, but do not consistently demonstrate subjective dystonic features. To determine whether striatal cholinergic interneuron excitation can cause potentially dystonic motor behaviors, we first determined features correlated specifically with dystonia severity in people and then determined whether these features emerged in mice following striatal cholinergic interneuron excitation.
Methods
Eight movement disorders experts rated dystonia severity in 193 videos of people with cerebral palsy doing a seated task. Leg adduction variability metrics, which are known to correlate with leg dystonia severity during gait, were quantified in these videos of seated tasks. Metrics significantly associated with leg dystonia severity during seated tasks in people were then quantified in mice and compared between mice who underwent chemogenetic striatal cholinergic interneuron excitation (n = 17) and mice who did not (n = 17).
Results
Leg adduction variability correlated well with experts' leg dystonia severity scores in people. Leg adduction variability was also significantly increased in mice that underwent striatal cholinergic interneuron excitation compared to mice that did not (p < 0.05). This difference was not present with acute excitation and emerged only after 14 days of ongoing excitation.
Interpretation
We demonstrate that leg adduction variability correlates with leg dystonia severity in people with cerebral palsy and that chronic, but not acute, striatal cholinergic interneuron excitation can cause leg adduction variability in mice. These results support targeting striatal cholinergic interneurons for dystonia drug development and demonstrate the potential value of using quantifiable leg adduction metrics to study dystonia pathophysiology. ANN NEUROL 2025;98:726–740
Sunday, November 9, 2025
Hydranencephaly
Alex Simpson turned 20-years-old Nov. 4, KETV reported.

Simpson’s parents had been told she was a healthy child until a check-up two months later revealed that their daughter had hydranencephaly – a rare condition that left her with just a pinky’s worth of brain matter at the base of her skull, the report said.
At the time, the Nebraska family were told Alex wouldn’t live past 4 years old.
“Twenty years ago we were scared, but faith, I think, is really what kept us alive,” Shawn Simpson, Alex’s father, told the TV station.
Though Alex is missing the parts of the brain capable of seeing and hearing, her family believes she’s more aware than people think.
“Say somebody’s stressed around her. Nothing will even happen — it could be completely silent — but Alex will know. She’ll feel something,” SJ, Alex’s 14-year-old brother, told the outlet.
“Like, if my grandma’s hurting, in her back, she’ll radiate off of it – it’s crazy,” he said.
SJ said he is proud to be Alex’s brother and has spent a lot of time researching her condition to learn how to support her.
Alex’s strength inspires the whole Simpson family, who call her a “miracle.”
Mikella Schuettler
https://nypost.com/2025/11/09/us-news/woman-born-with-no-brain-turns-20-in-medical-miracle/
Thursday, November 6, 2025
To become a syncope doctor
Wieling W. My good fortune to become a syncope doctor. Clin Auton Res. 2021 Feb;31(1):15-18. doi: 10.1007/s10286-020-00763-5. Epub 2021 Jan 8. PMID: 33417055.
Excerpt
Due to rapid advances in medical technology, molecular biology, genetics, clinical epidemiology, and evidence based medicine, as well as wide dissemination of electronic records and rapid turnover of patients, the interest in basic bedside medicine and clinical physiology has decreased. Nevertheless, the core bedside skills of careful history taking and physical examination, the backbone of clinical reasoning, remain vital for the evaluation of transient loss of consciousness (T-LOC) and syncope. The skill in diagnosing an unexplained episode of T-LOC/syncope starts with a meticulous documentation of what happened to deduce what is going on with this patient. The key to a successful syncope history is having sufcient knowledge to ask the right questions and taking enough time to listen to the patient intensely. History building with the patient instead of history taking from the patient is key. The patient needs to feel at ease and to trust the doctor, to reveal all important aspects underlying the episode, particularly the ones with psychosocial triggers. Some vital aspects of the history (which the patient may not consider important) need to be “teased out” by the doctor. This skill requires experience as well as a good interviewing technique. Careful history-taking and physiological reasoning are powerful tools to diagnose T-LOC and syncope. The diagnostic yield of a certain or highly likely diagnosis of T-LOC and syncope with history taking by hospital physicians is at least 60% with an accuracy of about 90%. The diagnostic yield can increase to as much as 85–95% with additional historytaking by a doctor with a special interest in syncope. Additional diagnostic testing increases the certainty of the diagnosis, but it does not contribute to improving patient care. The importance of history-taking and its high diagnostic yield implies that history taking must be allotted time. In complex cases, up to 1 h may be required.
A strong formal knowledge structure is needed for a successful interview of a patient with T-LOC and syncope. The Internet can serve as a strong educational tool for students and residents e.g. with a video-library with examples of episodes of reflex syncope. E-learning-based cases (eCases) are a far more effective tool for teaching than learning in a classroom listening to lectures. We have developed Syncopedia (www.syncopedia.org), a free-access educational website targeted at students, residents, and physicians to learn more about syncope. The website is an initiative of the Syncopedia Foundation, a non-proft organization established in the Netherlands in 2014. The goals of the Syncopedia Foundation are “to improve medical knowledge, especially in the field of syncope, and to provide access to this knowledge by facilitating publications in digital or other forms, for example by building and maintaining websites”. The goal of the Syncopedia website is to enhance physicians’ knowledge of syncope (or suspected syncope) and to reduce misdiagnosis, unnecessary testing, and multiple specialist consultations
Fetal monitoring and unnecessary caesarean section deliveries
But this round-the-clock monitoring, the most common obstetric procedure in the country, rarely helps baby or mother. Decades of research have shown that the tool does not reliably predict fetal distress. In fact, experts say, it leads to many unnecessary surgeries as doctors overreact to its ever-changing readouts.
The obstetrics field has long ignored these problems. Now, it’s putting more trust than ever on the flawed technology, often prioritizing business and legal concerns ahead of what’s best for patients, The New York Times found.
This fall, the American College of Obstetricians and Gynecologists updated its guidelines on continuous monitoring, sanctioning it even as some other wealthy countries have cautioned against its routine use. Some large hospitals have opened remote monitoring hubs, where nurses spend their shifts watching screens of pulsing squiggles beamed in from many miles away. Software companies have also jumped at the opportunity, selling unproven artificial intelligence algorithms that claim to pluck useful signals from the heartbeat noise.
All the while, the rate of cesarean sections in the United States remains stubbornly high. One out of every three deliveries happens in an operating room, a figure that far exceeds public health recommendations. The surgery can prolong a woman’s recovery, complicate future births and sometimes risk her life. The top justification for C-sections in healthy pregnancies is fetal distress, a diagnosis made by the monitor.
“We may be the only specialty that continues to do major abdominal surgery without a shred of evidence of benefit,” said Dr. Steven L. Clark, an obstetrician at Baylor College of Medicine in Texas who has extensively studied electronic monitoring. “We just plow blithely on.”
When electronic monitoring replaced simple stethoscope checks in the 1970s, doctors embraced it as a seemingly objective marker of how a birth was progressing. From the start, device companies pitched hospitals on an economic advantage: The tool allowed a single nurse to observe many patients at once.
On rare occasions, the fetal heartbeat can reveal when something has gone wrong. The trouble is, healthy babies have highly variable heart patterns. Since the introduction of continuous monitoring, doctors now have many more opportunities to mistakenly interpret these ambiguous signals as telltale signs of distress.
“Mostly it causes harm,” said Dr. Emmet Hirsch, an obstetrics professor at the University of Chicago Pritzker School of Medicine who has critiqued the approach in a leading medical journal. “It’s really the worst test in medicine.”
Other experts echoed his blunt assessment, with some calling the technology “useless” and “pathetic.”
Electronic monitoring is no more accurate than periodic stethoscope checks, studies have shown. But many obstetricians practicing today have never worked without a monitor. Some said they were convinced that the tool helped them practice better medicine, even if studies hadn’t shown it. Others felt that, with monitoring baked into hospital policies, the question of how patients might fare without it was moot.
“It’s just easier to keep patients hooked up continuously,” said Dr. Jon K. Hathaway, an obstetrician at Indiana University Health. “It’s an ease-of-manpower issue over the science.”
The technology has become pervasive in the courtroom, too. Several states have set recent records for malpractice verdicts with cases hinging on fetal monitoring. Highly paid expert witnesses point to the heart patterns in order to claim that a doctor missed warning signs of birth injuries like cerebral palsy, while defense witnesses use them to argue that nothing went amiss.
Some doctors said that although they were skeptical of monitoring, if they didn’t do it, a court could find them negligent.
‘What Could Be the Downside?’
The technology’s promise has long exceeded its capabilities.
Dr. Edward H. Hon, an obstetrician at Yale, began studying fetal heart patterns in the 1950s, trying to find markers of oxygen deprivation. In one case report of an infant born too premature to survive, he claimed to have found a distinctively slow heartbeat many hours before death.
The Epsco Medical company soon debuted the “Hon Fetal Monitor,” a tall box that spit out heart patterns on long strips of paper. In the early 1960s, the machine cost $9,950, or more than $100,000 in today’s dollars.
Advertisements in medical journals at the time said the monitor gave the “earliest possible warning” of heart deviations. “Hopefully, Dr. Hon’s new system could save as many as 20,000 babies a year,” Life magazine wrote in 1969.
But when Dr. Hon published data on his device the next year, he sounded a cautious note. His study found that 252 high-risk patients at Yale had modestly positive birth outcomes when using the monitor but noted that a “sizable, carefully controlled study” was still needed to prove its effectiveness.
Early critics warned that any screen looking for events as rare as death and brain injury was doomed to pick up false positives. Nevertheless, doctors adopted electronic monitoring with fervor.
“The thought was, ‘What could be the downside of this?’” said Jacqueline Wolf, a medical historian at Ohio State University.
Manufacturers trumpeted how their monitors could stand in for hospital staff, according to dozens of ads archived at the National Library of Medicine in Bethesda, Md.
“One person can continuously and simultaneously monitor eight patients,” read an ad in 1970. Another, from 1980, claimed that a monitor was “like keeping a nurse at every bedside.”
The technology’s uptake coincided with a drop in stillbirth rates, and some hospitals published studies attributing the improvement to electronic monitors. But a clinical trial that randomly assigned women to the device, published in 1976, found no improvement in the number of newborn deaths or other negative outcomes. A government report concluded that other changes, like the advent of neonatology as a specialty, better nutrition and fewer young women giving birth, probably drove the stillbirth decline.
That first trial, as well as a large follow-up, also reported a significant harm of the technology: a far higher rate of C-sections.
The machines grew more popular even as large studies demonstrated their futility. In 1996, the United States Preventive Services Task Force gave electronic monitoring its lowest grade, “D,” and discouraged its use in healthy pregnancies. Doctors seemed to pay no mind.
A rigorous review in 2017 found that compared with stethoscope monitoring, the electronic version did not reduce stillbirths or cerebral palsy, a neurological disorder sometimes caused by oxygen deprivation before birth. The tool did decrease rare neonatal seizures, though that did not change the baby’s risk of neurological injuries later on.
And the technology increased a woman’s odds of cesarean delivery by 63 percent, the review found.
Cesarean rates in the United States began to soar in the 1970s and have exceeded public health targets for years. The surgeries come with a host of medical risks to the mother, including hemorrhage and infection.
The primary justification for C-sections among women with healthy pregnancies is “fetal distress,” a diagnosis nearly always based on the monitor, according to a recent study of 40 million births.
“Electronic fetal monitoring, as a single entity, has probably driven up the C-section rate more than anything else,” said Dr. George A. Macones, who directs women’s health at Dell Medical School in Texas and has long studied monitoring.
Cesareans for fetal distress
Fetal distress is the most common reason that C-sections are performed in healthy pregnancies.
When Sanquaneice Hankerson-Pinkney went into labor in March 2021, her doctor advised a cesarean based on the fetal heart rate. She readily agreed.
“Seeing the heart rate dropping on the monitor, it made me sick to my stomach,” said Ms. Hankerson-Pinkney, 37, a lawyer in Lauderdale Lakes, Fla.
When she got pregnant again the next year, her placenta grew into the scar tissue left on her uterus from the surgery — a life-threatening condition that, while rare, has become more prevalent as C-sections have risen.
Because the two organs were entwined, natural labor could have killed Ms. Hankerson-Pinkney. So she delivered five weeks early, and the infant was put on a breathing machine. When doctors could not wrest the placenta out of Ms. Hankerson-Pinkney, they removed the entire fused uterus, dashing her hopes of more children.
“It was more traumatic than I would like to express,” she said.
Ms. Hankerson-Pinkney may never know whether her first C-section was warranted. The hospital where she delivered, Plantation General, has since closed. Its parent company, HCA Healthcare, said that C-section decisions were made carefully after discussions between doctors and patients.
“Each delivery involves unique clinical factors, including the mother’s age, body mass index, any pre-existing conditions and potential distress of the baby indicated by the fetal heart tones,” the company said in a statement.
The obstetrician overseeing that surgery, Dr. Jay S. Cohen, had a 63 percent cesarean rate in 2023, about double the national average, according to the most recent data available from Florida’s Health Department.
Dr. Cohen said his practice attracted a “very high-risk population” that other doctors turn away. As for Ms. Hankerson-Pinkney, he said, “I think she was very happy with the care she got.”
Obstetricians are more likely to get sued than doctors in any other medical specialty. Monitoring records often become critical evidence, with expert witnesses on each side offering competing interpretations.
“It’s very squishy,” said Amy Collignon Gunn, a partner at Gunn Slater in St. Louis. “You get a lot of subjective reading.”
In July, Ms. Gunn represented a Missouri family who won $48 million — the state’s largest malpractice verdict in decades — after using monitoring records to claim that a hospital was responsible for a baby’s cerebral palsy.
In a similar case that month, a Pennsylvania court ordered a hospital to pay $207 million. A Utah judge went even higher in August, awarding $950 million to the family of a brain-injured baby.
No studies have shown that performing a cesarean based on fetal heart patterns can prevent cerebral palsy. Yet expert witnesses often point to monitor readings to claim a doctor was negligent.
Dr. Michael Cardwell, a retired obstetrician in Columbia, Mo., said he had consulted on more than 600 cases in his 40-year career, almost always testifying against doctors. He charges $700 an hour to review documents, and $12,000 to $15,000 for a day of trial testimony.
At least two courts, in Arizona and Maryland, have rejected his opinions about fetal monitoring in recent years because he did not provide research to back up his claims.
Dr. Cardwell said he did not know that his testimony in those cases had been excluded, and that it rarely happened. Sometimes, he said, courts “try to use evidence-based medicine to an extreme point of view.”
Dr. Cardwell was the family’s expert witness in the record-breaking Pennsylvania case, which an appeals court upheld in July. He and a defense witness offered wholly different interpretations of the same monitoring strip.
He told the jury that the baby would not have been injured if doctors had delivered him around 1:30 p.m. instead of 2:30 p.m.
“What is the baby telling us here?” the family’s lawyer asked Dr. Cardwell, referring to a spot in the readout before 2:30 p.m.
“The baby is telling you, ‘I’m not getting enough oxygen,’” the doctor responded.
The defense’s witness, Dr. Laura Goetzl, an obstetrician at the University of Texas, testified that the records did not indicate an emergency. She said the baby’s brain injury was probably the result of inflammation from a uterine infection that both sides agreed had occurred. An umbilical cord test, she said, had found a normal fetal oxygen level.
In a brick office building outside Baltimore, nurses with the University of Maryland Medical System sit day and night watching screens of fetal heart data from seven hospitals as far as 60 miles away.
“With cutting-edge A.I. technology, we are setting the highest benchmarks for safety and equity,” a news release boasted after the monitoring hub opened last year.
A growing number of hospitals have opened such facilities, often making claims about patient safety. The Ochsner Health system in Louisiana has said that its remote hub reduced admissions to neonatal intensive care. But a 2021 study by Ochsner’s own researchers found that was not true. (The study did find a slight drop in C-sections, though statewide rates were also declining during the same period.)
An Ochsner spokeswoman said the claims about improved NICU admissions were based on “internal data.”
The hubs have also helped lower costs, hospital executives told The Times.
At OhioHealth, which opened the country’s first remote monitoring facility in 2013, the extra layer of expertise has made administrators more comfortable hiring nurses with less experience on labor and delivery floors, said Dr. Jason V. Melillo, the hospital’s vice president for women’s health. That change has been particularly helpful, he said, given the nursing shortage.
At the same time, OhioHealth’s leaders believe the hub has helped cut malpractice costs. They estimated saving $13.5 million in its first two years, based on how often nurses intervened in cases that executives predicted would have otherwise resulted in a lawsuit.
The facility also helps with optics in legal disputes because it suggests that a hospital took every effort to prevent harm, said Bobbie Sprader, a lawyer who has worked with OhioHealth. “It just looks good, and that sometimes matters more than about anything,” she said in an August webinar for executives.
All three remote hubs, along with 400 other hospitals around the country, use A.I. software to help analyze the heart data. The software’s maker, PeriGen, has claimed on its website that 50 studies backed up its products.
But none of the studies found that the technology improved birth outcomes. One described how to suture a cesarean scar.
PeriGen removed the list of studies after an inquiry from The Times. The company’s chief executive, Matthew Sappern, acknowledged that no clinical trials had shown benefits. “It certainly is not our intent to be misleading,” he said.
In its newly updated guidelines, the American College of Obstetricians and Gynecologists said A.I. software for fetal monitoring was unproven.
But the organization — which has over 60,000 members and enormous influence over how they practice — supported continuous monitoring, even while acknowledging that evidence for the tool was “inadequate.” Obstetric guidelines in Canada and Britain, in contrast, have recommended against routine use of the tool in healthy pregnancies.
When asked why the American guidelines approved of electronic monitoring despite the lack of evidence, Dr. Aaron B. Caughey, an obstetrician who co-wrote the guidelines, said that the research wasn’t perfect and clinical experience also mattered.
When he learned in medical school about the technology’s bad track record, he was horrified, he said. But over 30 years in practice, he has found the tool helpful. He hangs his hat on the older studies that showed a benefit. Those that have not, he said, might have simply been too small to prove it.
“The practice of obstetrics is hard in 2025,” he said. “But I think that this tool continues to be of use.”
Sarah Kliff
https://www.nytimes.com/2025/11/06/health/electronic-fetal-monitoring-c-sections.html?auth=login-google1tap&login=google1tap&smid=url-share&unlocked_article_code=1.zE8.QNuT.wxhXOlyuePSf
Wednesday, November 5, 2025
Trends in prenatal exposure to antiseizure medications over the past decade
Abstract
Background and objectives: Prenatal exposure to certain antiseizure medications (ASMs) is associated with established or suspected risks of congenital malformations and neurodevelopmental disorders. Large-scale, real-life data are essential to guide efforts to mitigate these risks. Our objective was to assess trends in prenatal exposure to ASMs over the past decade according to medication safety profiles.
Methods: This nationwide, population-based study is based on comprehensive data of the French National Mother-Child Register EPI-MERES. All ASM-exposed pregnancies ended between 2013 and 2021 were included. ASM-exposed pregnancies' frequency and characteristics (maternal sociodemographics and morbidities, pregnancy outcome, and ASM treatment modalities) were assessed considering 3 safety categories: (1) ASMs considered the safest (lamotrigine and levetiracetam); (2) ASMs with uncertain risk, including pregabalin, gabapentin, and newer ASMs (e.g., lacosamide and zonisamide); and (3) ASMs with acknowledged risk, including valproic acid, valpromide, carbamazepine, and topiramate.
Results: Between 2013 and 2021, 55,801 pregnancies were exposed to ≥1 ASM. Pregnancies exposed to the safest ASMs increased by +30%. Meanwhile, prenatal exposure to valproic acid and valpromide dramatically decreased due to decreasing numbers of exposed pregnancies (-84% and -89%, respectively), increasing termination rate of exposed pregnancies (+23% and +28%, respectively), and among those ended in childbirth, decreasing numbers with multiple valproate dispensations (-86% and -93%, respectively) or sustained exposure throughout pregnancy (-91% and -96%, respectively). Prenatal exposure to carbamazepine and topiramate barely decreased, with almost 600 newborns still exposed to each of these ASMs in 2019-2021. Pregabalin and gabapentin became widely used during pregnancy, resulting in more and more newborns prenatally exposed (+28%), and for pregabalin increasingly with multiple dispensations (+65%) and sustained exposure throughout pregnancy (+171%). The numbers of pregnancies and newborns exposed to newer ASMs also sharply increased (+140% and +60%, respectively). Overall, prenatal exposure to ASMs with acknowledged or uncertain risk disproportionately concerned pregnant women with a low level of resources (18.5% and 17.9%, respectively, vs 13%-14% among pregnancies exposed to the safest ASMs or ASM-unexposed).
Discussion: Despite a sharp shift from valproate to safer ASMs, prenatal exposure to other ASMs with acknowledged or uncertain risks has persisted or even increased, particularly among the most socially disadvantaged populations, requiring additional risk minimization measures.
Abstract
Background and objectives: Maternal use of first-generation antiseizure medications (ASMs), such as valproate and phenobarbital, increases the risk of congenital malformations in offspring. Second-generation ASMs, such as lamotrigine and levetiracetam, pose less risk to fetal development, although topiramate seems to increase the risk of oral clefts. Less is known about the safety of newer second-generation ASMs during pregnancy including oxcarbazepine, zonisamide, and lacosamide. The aim of this study was to quantify the relative risk of major malformations in offspring after maternal use of specific ASMs early in pregnancy, with special interest in second-generation ASMs.
Methods: The study population included pregnant women who enrolled in the North American Antiepileptic Drug Pregnancy Registry between 1997 and 2023. Data on ASM use and maternal characteristics were collected through phone interviews at enrollment, at 7 months of gestation, and within 3 months after delivery. Malformations were confirmed by medical records and adjudicated by a dysmorphologist. The risk of major malformations was estimated among infants exposed to specific ASMs in monotherapy during the first trimester of pregnancy. Risk ratios (RRs) and 95% CIs were estimated with logistic regression models.
Results: A total of 7,311 participants taking an ASM as monotherapy during the first trimester were eligible for analysis. The mean age was 30 years. The risk of major malformations was 2.1% (52/2,461) for lamotrigine, 2.0% (26/1,283) for levetiracetam, 2.8% (32/1,132) for carbamazepine, 5.1% (26/510) for topiramate, 2.8% (12/423) for phenytoin, 9.2% (31/337) for valproate, 1.5% (5/327) for oxcarbazepine, 1.5% (4/270) for gabapentin, 1.3% (3/228) for zonisamide, 6.0% (12/200) for phenobarbital, 3.2% (2/62) for pregabalin, and 0% (0/88) for lacosamide. Compared with lamotrigine, the RR was 5.1 (95% CI 3.0-8.5) for valproate, 2.9 (1.4-5.8) for phenobarbital, and 2.2 (1.2-4.0) for topiramate. Topiramate was specifically associated with a higher risk of cleft lip.
Discussion: Results confirm the association between maternal use of valproate, phenobarbital, and topiramate early in pregnancy and a higher risk of major malformations in the infant compared with lamotrigine. However, they do not support meaningful risk elevation for levetiracetam, oxcarbazepine, gabapentin, or zonisamide. Relative risk estimates for lacosamide and pregabalin are still imprecise.
Tuesday, November 4, 2025
Autism and leucovorin
Wells L, O'Hara N, Frye RE, Hullavard N, Smith E. Folate Receptor Alpha Autoantibodies in the Pediatric Acute-Onset Neuropsychiatric Syndrome (PANS) and Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS) Population. J Pers Med. 2024 Jan 31;14(2):166. doi: 10.3390/jpm14020166. PMID: 38392599; PMCID: PMC10890663.
Abstract
The folate receptor alpha autoantibodies (FRAAs) are associated with cerebral folate deficiency (CFD) and autism spectrum disorder (ASD). Both of these syndromes have overlapping characteristics with Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS) and Pediatric Acute-Onset Neuropsychiatric Syndrome (PANS). Thus, we propose that the FRAAs may contribute to the symptomatology of PANS/PANDAS. To test this hypothesis, 1 mL of serum from 47 patients (age range = 6–18 years old) clinically diagnosed with PANS/PANDAS was sent to Vascular Strategies (Plymouth Meeting, PA, USA) for analysis of FRAAs. Moreover, 63.8% of PANS/PANDAS patients (male = 15; female = 15) were found to have either the blocking and/or blinding FRAAs, with 25 (83.3%; male = 14; female = 11) having binding FRAAs, two (6.7%; all female = 2) having blocking FRAAs, and 3 (10%; male = 1; female = 2) having both binding and blocking. Furthermore, surprisingly, ASD was associated with a 0.76 lower binding titer (p = 0.02), and severe tics were associated with a 0.90 higher binding titer (p = 0.01). A case of a FRAA-positive patient is provided to illustrate that a treatment plan including leucovorin can result in symptom improvement in patients with PANS/PANDAS who are FRAA-positive. These data, for the first time, demonstrate that PANS/PANDAS is associated with FRAAs and suggest folate metabolism abnormalities may contribute to PANS/PANDAS symptomatology. Further studies investigating the therapeutic nature of leucovorin in the treatment of PANS/PANDAS are needed. Such studies may open up an alternative, safe, and well-tolerated treatment for those with the PANS/PANDAS diagnosis.
Rossignol DA, Frye RE. Cerebral Folate Deficiency, Folate Receptor Alpha Autoantibodies and Leucovorin (Folinic Acid) Treatment in Autism Spectrum Disorders: A Systematic Review and Meta-Analysis. J Pers Med. 2021 Nov 3;11(11):1141. doi: 10.3390/jpm11111141. Erratum in: J Pers Med. 2022 Apr 29;12(5):721. doi: 10.3390/jpm12050721. PMID: 34834493; PMCID: PMC8622150.
Abstract
The cerebral folate receptor alpha (FRα) transports 5-methyltetrahydrofolate (5-MTHF) into the brain; low 5-MTHF in the brain causes cerebral folate deficiency (CFD). CFD has been associated with autism spectrum disorders (ASD) and is treated with d,l-leucovorin (folinic acid). One cause of CFD is an autoantibody that interferes with the function of the FRα. FRα autoantibodies (FRAAs) have been reported in ASD. A systematic review was performed to identify studies reporting FRAAs in association with ASD, or the use of d,l-leucovorin in the treatment of ASD. A meta-analysis examined the prevalence of FRAAs in ASD. The pooled prevalence of ASD in individuals with CFD was 44%, while the pooled prevalence of CFD in ASD was 38% (with a significant variation across studies due to heterogeneity). The etiology of CFD in ASD was attributed to FRAAs in 83% of the cases (with consistency across studies) and mitochondrial dysfunction in 43%. A significant inverse correlation was found between higher FRAA serum titers and lower 5-MTHF CSF concentrations in two studies. The prevalence of FRAA in ASD was 71% without significant variation across studies. Children with ASD were 19.03-fold more likely to be positive for a FRAA compared to typically developing children without an ASD sibling. For individuals with ASD and CFD, meta-analysis also found improvements with d,l-leucovorin in overall ASD symptoms (67%), irritability (58%), ataxia (88%), pyramidal signs (76%), movement disorders (47%), and epilepsy (75%). Twenty-one studies (including four placebo-controlled and three prospective, controlled) treated individuals with ASD using d,l-leucovorin. d,l-Leucovorin was found to significantly improve communication with medium-to-large effect sizes and have a positive effect on core ASD symptoms and associated behaviors (attention and stereotypy) in individual studies with large effect sizes. Significant adverse effects across studies were generally mild but the most common were aggression (9.5%), excitement or agitation (11.7%), headache (4.9%), insomnia (8.5%), and increased tantrums (6.2%). Taken together, d,l-leucovorin is associated with improvements in core and associated symptoms of ASD and appears safe and generally well-tolerated, with the strongest evidence coming from the blinded, placebo-controlled studies. Further studies would be helpful to confirm and expand on these findings.
Frye RE, McCarty PJ, Werner BA, Scheck AC, Collins HL, Adelman SJ, Rossignol DA, Quadros EV. Binding Folate Receptor Alpha Autoantibody Is a Biomarker for Leucovorin Treatment Response in Autism Spectrum Disorder. J Pers Med. 2024 Jan 1;14(1):62. doi: 10.3390/jpm14010062. PMID: 38248763; PMCID: PMC10820361.
Abstract
Autism spectrum disorder (ASD) affects up to 1 in 36 children in the United States. It is a heterogeneous neurodevelopmental disorder with life-long consequences. Patients with ASD and folate pathway abnormalities have demonstrated improved symptoms after treatment with leucovorin (folinic acid), a reduced form of folate. However, biomarkers for treatment response have not been well investigated and clinical trials are lacking. In this retrospective analysis, a cohort of prospectively collected data from 110 consecutive ASD clinic patients [mean (SD) age: 10.5 (6.2) years; 74% male] was examined. These patients all underwent testing for folate receptor alpha autoantibodies (FRAAs) and soluble folate binding proteins (sFBPs) biomarkers and were treated with leucovorin, if appropriate. Analyses examined whether these biomarkers could predict response to leucovorin treatment as well as the severity of ASD characteristics at baseline. The social responsiveness scale (SRS), a measure of core ASD symptoms, and the aberrant behavior checklist (ABC), a measure of disruptive behavior, were collected at each clinic visit. Those positive for sFBPs had more severe ASD symptoms, and higher binding FRAA titers were associated with greater ABC irritability. Treatment with leucovorin improved most SRS subscales with higher binding FRAA titers associated with greater response. Leucovorin treatment also improved ABC irritability. These results confirm and expand on previous studies, underscore the need for biomarkers to guide treatment of folate pathways in ASD, and suggest that leucovorin may be effective for children with ASD.
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