Brown v Meaney: Pyridoxine, Informed Consent, and the Low-Risk Alternative

Some malpractice cases turn on a single uncomfortable feature of the clinical record. The physicians did consider the right diagnosis. The diagnosis was uncommon enough to be hard to confirm. There was a treatment that worked. The treatment was inexpensive, widely available, and had essentially no adverse effects. The physicians did not maintain the treatment. The patient continued to seize. Permanent brain injury followed.

Brown v Meaney, 2024 ONSC 7256, is a case in that category. Justice Michael Bordin of the Ontario Superior Court of Justice released the decision on December 30, 2024. The trial judge found that two pediatric neurologists at McMaster Children’s Hospital in Hamilton had been negligent in the treatment of Skyler Brown, an infant who had begun experiencing seizures at four months of age. The negligence consisted principally of the failure to maintain pyridoxine (vitamin B6) treatment for a condition that turned out to be pyridoxine-dependent epilepsy (PDE) — a rare genetic disorder in which seizures cannot be controlled by ordinary antiepileptic medications but can be controlled by pyridoxine, a vitamin available at essentially any pharmacy in Canada for cents per dose.

The trial judge also found a separate breach of the duty to obtain informed consent. The parents were not adequately informed about the pyridoxine trial, about the decision to discontinue B6, or about the importance of restarting B6 if seizures returned. The mother’s evidence at trial established that, had the necessary information been provided, she would not have consented to discontinuing B6 and would have insisted on restarting it when the seizures returned. The modified objective test for informed consent causation was satisfied.

Skyler’s twin sister Summer also has PDE. She received early and consistent pyridoxine treatment. She improved. The comparison between the two sisters operated as a natural experiment on causation that the defence was unable to overcome at trial. The trial judge found that the defendants’ negligence caused or contributed to the brain injury, the intellectual and developmental delay, and the developmental challenges Skyler faces.

The case is a clean plaintiff-success Ontario decision that articulates several doctrinal frameworks of practical importance: the rejection of the “rare disease” defence to negligence; the “low-risk alternative” framework that operates when a safe and effective treatment is available but not used; the limits of “common practice” as a defence to a negligence claim; the informed consent framework as it operates in pediatric care where parents are the decision-makers; and the use of natural experiments (in this case, the twin sister) as causation evidence.

The clinical context: pyridoxine-dependent epilepsy

A brief clinical overview is necessary to make sense of the legal analysis.

The disease. Pyridoxine-dependent epilepsy is a rare autosomal recessive genetic disorder caused by mutations in the ALDH7A1 gene. The mutations produce a deficiency of the enzyme antiquitin, which is involved in the lysine metabolism pathway. The deficiency produces accumulation of metabolites that depress brain function and produce seizures.

The presentation. PDE most commonly presents in the neonatal or early infant period with seizures that are intractable to standard antiepileptic medications (phenobarbital, phenytoin, levetiracetam, and others). The seizures do not respond to typical first-line treatments and continue despite appropriate dose escalations.

The treatment. PDE is one of the very few causes of intractable infantile epilepsy that responds to a specific and simple intervention: pyridoxine supplementation. The dose required is substantially higher than the recommended daily allowance of vitamin B6 (typically 30-100 mg per day in infants, compared with the dietary requirement of 0.1-0.5 mg per day), but the treatment is essentially without significant adverse effects at the doses required. Pyridoxine is available in any Canadian pharmacy as an over-the-counter supplement.

The diagnostic challenge. Before genetic testing became widely available, PDE was diagnosed by therapeutic trial: pyridoxine was administered, and if the seizures responded, the diagnosis was supported. A more definitive diagnosis became possible with biochemical testing (measurement of alpha-aminoadipic semialdehyde, AASA, in the urine) and ultimately genetic testing for ALDH7A1 mutations.

The clinical urgency. Untreated PDE causes recurrent seizures during a period of rapid brain development. The seizures themselves contribute to brain injury through excitotoxicity, hypoxic stress, and disruption of normal neural development. The longer treatment is delayed, the greater the cumulative injury. Early treatment with pyridoxine can prevent or substantially reduce the long-term neurodevelopmental consequences.

The clinical context is the foundation for the legal analysis. PDE is rare. The diagnosis is not always obvious in the early months. But the treatment is simple, safe, and effective. The cost of trying the treatment is essentially zero. The cost of not trying it, when it would have worked, is permanent and severe.

The facts as found

The patient. Skyler Brown was born in December 2002. She was an apparently healthy term newborn. Her twin sister Summer was also born healthy. In April 2003, when Skyler was approximately four months old, she developed seizures.

The initial response. Skyler was seen at hospital, treated with medications, and referred to a pediatrician. The seizures continued despite management. She was readmitted with increased seizure frequency and severity.

The pyridoxine trial. As part of the workup for intractable infantile seizures, the physicians initiated a pyridoxine trial. In early May 2003, Skyler was given pyridoxine and her seizures appeared to respond. On May 16, 2003, the physicians discontinued the pyridoxine. The clinical decision was a routine one in the context of a therapeutic trial: if the patient is seizure-free on pyridoxine, the physicians need to determine whether the response is due to the pyridoxine specifically (in which case the diagnosis is PDE and pyridoxine should continue) or due to other factors (in which case pyridoxine could be discontinued without consequence). The discontinuation is the test.

The recurrence. On May 26, 2003, ten days after the pyridoxine was discontinued, Skyler’s seizures returned. The physicians’ response to this recurrence is at the heart of the case. They did not restart pyridoxine. They continued with other antiepileptic medications. The seizures continued. The clinical course progressed through escalating interventions including a ketogenic diet.

The medically induced coma. In July 2003, Skyler’s seizures had reached a severity that prompted the physicians to induce a medical coma to control them. The coma was used as a clinical intervention for status epilepticus that had not responded to other treatments. Coma at this point in a five- to seven-month-old infant produced substantial additional risk.

The recovery and the eventual diagnosis. Skyler eventually came off the medical coma. A new medication regimen including pyridoxine was established and the seizures came under control. Subsequent attempts to discontinue the pyridoxine produced seizure recurrence, confirming clinically what the physicians had not concluded in 2003: that Skyler’s seizures were pyridoxine-dependent. Genetic testing in 2008 confirmed the PDE diagnosis. As of the trial period, Skyler had been managed on pyridoxine and dietary therapy with substantial seizure control.

The twin sister. Skyler’s twin sister Summer also has PDE. The genetic basis means that the two sisters had the same underlying disease at the same time. Summer received early and consistent pyridoxine treatment. She had a different developmental trajectory: improved, more typical neurodevelopment, far fewer of the catastrophic features that Skyler experienced. The two sisters provide a natural experiment: same disease, same family, same environment, different treatment, different outcome. The natural experiment is rare in malpractice litigation and is particularly powerful as evidence of causation.

The injury. Skyler suffers severe neurologic injuries and intellectual and developmental delay. She faces lifelong developmental challenges.

The legal framework — standard of care

The trial judge worked through the standard of care analysis in several distinct components.

The failure to implement a monotherapy trial before May 20, 2003. The standard of practice in pediatric neurology for an infant with intractable seizures includes a structured approach to trial of treatments. A monotherapy trial — where a single antiepileptic is used in isolation to assess its effect — is the foundation of the diagnostic process. The trial judge found that the defendants had not implemented a monotherapy trial before May 20, 2003. The failure was a breach of the standard of care.

The insufficient observation period after discontinuing pyridoxine on May 16, 2003. When pyridoxine is discontinued as part of a therapeutic trial for PDE, the observation period required to confirm or rule out the diagnosis is a defined clinical question. The defendants’ observation period was found by the trial judge to be insufficient. The implication: a longer observation period (or a different protocol entirely) would have allowed earlier identification that pyridoxine was the necessary treatment.

The failure to consider restarting pyridoxine when seizures recurred. This is the central breach in the case. When Skyler’s seizures returned on May 26, 2003 (ten days after pyridoxine had been discontinued), the appropriate clinical response was to consider that the temporal relationship pointed to pyridoxine-dependent seizures and to restart the pyridoxine to test that hypothesis. The defendants did not do this. They continued with other antiepileptic medications. The trial judge found that this was a breach of the standard of care.

The “blindly following common practice” finding. The defendants argued that their approach was consistent with common practice for atypical PDE in 2003. The trial judge addressed this argument directly. He found that the defendants had “blindly followed a common practice” that was “fraught with obvious risk” rather than administering “an innocuous vitamin like pyridoxine which could have mitigated severe risks without causing harm.” The framing is doctrinally important: common practice is not in itself a complete defence to a negligence allegation. Where the common practice is itself questionable, and where a low-risk alternative exists, common practice does not shield the physician from a finding of negligence.

The framework parallels the Supreme Court of Canada’s articulation in ter Neuzen v Korn, [1995] 3 SCR 674: a court can find a common practice to be negligent if the practice is itself fraught with obvious risk. The proposition is well-settled. Brown v Meaney applies it specifically in the context of pediatric neurology where a low-risk alternative was available.

The legal framework — informed consent

The trial judge separately found a breach of the duty of informed consent.

The framework. The Canadian informed consent framework was established by the Supreme Court of Canada in Reibl v Hughes, [1980] 2 SCR 880, and Hopp v Lepp, [1980] 2 SCR 192. The framework requires the physician to inform the patient (or, in pediatric care, the parents acting for the patient) of:

• The diagnosis and the proposed treatment
• The material risks of the proposed treatment, including those associated with the treatment itself and those associated with not having the treatment
• The alternatives to the proposed treatment
• The expected consequences of each option

The “material” risk is a risk that a reasonable patient in the circumstances would want to know about. The threshold is patient-specific rather than purely clinical.

Causation in informed consent. The modified objective test for informed consent causation (also from Reibl v Hughes) asks: would a reasonable person in the patient’s position, properly informed, have made a different decision? The test is subjective in its consideration of the patient’s specific circumstances but objective in its assessment of what a reasonable person in those circumstances would have done.

The breach. The trial judge found that the defendants failed to provide information to Skyler’s parents about:

• The pyridoxine trial and its significance
• The decision to discontinue B6 and the basis for that decision
• The potential risks, benefits, and alternatives
• The importance of restarting pyridoxine if seizures resumed

The causation. The mother’s testimony at trial established that, had she been adequately informed:

• She would not have consented to discontinuing the B6 on May 16, 2003
• She would have immediately restarted the B6 (or queried the doctors about restarting it) when the seizures returned on May 26, 2003

The trial judge accepted this testimony and found that the modified objective test was met: any reasonable person in the parents’ position, properly informed, would very likely have continued the B6 and would not have agreed to discontinue it.

The two findings (the SOC breach and the informed consent breach) operate independently. Either one would have supported liability. Together they form a comprehensive finding that the defendants failed both their technical and their relational obligations to the patient and her family.

The legal framework — causation

The causation analysis is where the twin sister comparison did much of the work.

The plaintiff’s case. The plaintiff established that:

• Skyler had been developing normally before the May 2003 events
• The repeated brain-injuring seizures and the medically induced coma during the relevant period were the principal mechanism of brain injury
• The brain injury produced the intellectual and developmental delay Skyler now faces
• Earlier and consistent pyridoxine treatment would have prevented the seizures from continuing
• The trajectory of Skyler’s twin sister Summer (who received early pyridoxine treatment and had a much better neurodevelopmental outcome) provided direct comparative evidence on what the appropriate clinical course could have produced

The defendants’ case. The defendants argued:

• PDE is a neurodevelopmental disorder; some developmental challenges may be intrinsic to the condition
• Variations in developmental outcomes among PDE patients exist independent of treatment timing
• The robust evidence base in PDE studies is limited (the disease is rare)
• The expert opinions did not reach consensus on the precise impact of pyridoxine treatment timing

The defendants’ argument was essentially that the outcome would have been the same regardless of when pyridoxine was started — that Skyler’s neurodevelopmental challenges were intrinsic to her PDE rather than caused by the treatment delay.

The trial judge’s analysis. The trial judge rejected the defendants’ causation argument. The reasoning, distilled:

• The regression in Skyler’s development after July 6, 2003 (when the medical coma was induced) was striking and contemporaneous with the acute clinical events
• The slowdown in brain growth (as evidenced by serial imaging and clinical assessment) correlated with the period of inadequately treated seizures
• The comparison with the twin sister Summer (same disease, different treatment, better outcome) provided direct evidence that early pyridoxine treatment makes a substantial difference
• The plaintiff had successfully established a probable causal link between the breaches and the injury

The causation finding is doctrinally important because of the twin sister evidence. In most malpractice cases, the trier of fact must construct a counterfactual: what would have happened if the standard of care had been met? The construction is necessarily speculative; it relies on expert evidence about typical clinical pathways and on inferences about how this patient specifically would have responded. In Brown v Meaney, the counterfactual was less speculative. Summer’s actual trajectory provided direct evidence about what Skyler’s trajectory could have been with appropriate treatment.

The doctrinal anchors

Several doctrinal anchors emerge from the case.

The rejection of the “rare disease” defence. The defendants argued that PDE was rare and not well-known and that their treatment decisions should be assessed against that context. The trial judge accepted that PDE is rare but rejected the argument that the rarity excused the breach. The framework: rarity affects what reasonable physicians can be expected to recognize, but it does not affect the standard of care once a particular treatment is being considered. The physicians were considering pyridoxine; they did a trial; they got an apparent positive response; they discontinued; the seizures recurred. The clinical pattern that follows from that sequence is the same regardless of the disease’s prevalence. The rare disease defence is bounded.

The “low-risk alternative” framework. The case is a clean illustration of a recurring doctrinal pattern: where a low-risk alternative is available and clinically appropriate, the failure to use it is a more obvious breach of the standard of care. Pyridoxine is essentially a vitamin. It has no significant adverse effects at the doses required for PDE. Its cost is negligible. The trial judge framed this directly: the defendants chose to “blindly follow a common practice” rather than “administer an innocuous vitamin like pyridoxine which could have mitigated severe risks without causing harm.”

The framework is generalizable. In any case where a low-risk and inexpensive intervention is available and might address the clinical question, the failure to use it is harder to defend than the failure to use an intervention with significant risk or cost. The trade-off analysis that supports clinical conservatism in high-risk interventions does not operate when the intervention has essentially no downside.

The “blindly following common practice” doctrine. Common practice is a defence to negligence in some circumstances. Where physicians follow the prevailing approach in their specialty, they have an argument that they have met the standard of care. But the defence is bounded. Ter Neuzen v Korn, [1995] 3 SCR 674, establishes that a common practice can itself be negligent if the practice is “fraught with obvious risk.” The trial judge in Brown v Meaney applied this framework: the common practice of waiting to confirm PDE before resuming pyridoxine, in a context where seizures were continuing and where pyridoxine had no significant downside, was “fraught with obvious risk.” Common practice did not save the defendants.

The informed consent framework with low-risk alternatives. The informed consent obligation is particularly important where a low-risk alternative is available. The patient (or in pediatric care, the parents) needs to know that the alternative exists, what its risks and benefits are, and how it compares to the proposed treatment. Where the alternative is essentially without risk, the failure to disclose it is a particularly clear breach. The mother’s testimony in Brown v Meaney directly demonstrated the causation: with full information about pyridoxine as a low-risk option, she would not have consented to discontinuing it.

The natural experiment as causation evidence. The twin sister Summer provided an unusually direct causation comparison: same disease, same family, same environment, different treatment, different outcome. Natural experiments of this kind are rare in malpractice litigation. Where they exist, they substantially strengthen the plaintiff’s causation case. The framework is generalizable: any case in which the plaintiff can identify a contemporaneous comparable patient (a sibling, a member of the same diagnostic cohort, a patient treated by a different provider for the same condition) can be substantially advanced by the comparison. The principle is not specific to twin sisters; it applies wherever direct evidence of the alternative trajectory is available.

The breach without causation pattern in reverse. The cluster’s “breach without causation” pattern (illustrated in Williamson, Papineau, Lorencz, Yang) operates against plaintiffs where the counterfactual analysis cannot be sustained. Brown v Meaney is the inverse: the counterfactual was clearly supported by the comparative evidence, and the causation analysis succeeded. The case demonstrates that where the counterfactual can be supported by direct evidence rather than reconstruction, the plaintiff’s case is structurally stronger.

The pediatric malpractice context

A few observations about the pediatric malpractice context that frame the case.

The parents as decision-makers. In pediatric care, the patient cannot consent. The parents (or other guardians) consent on the patient’s behalf. The informed consent obligation runs to the parents. The framework engages two relational dimensions: the physician-patient relationship (with the child) and the physician-parent relationship (with the consent-givers). Both must be managed appropriately. Brown v Meaney illustrates the consequences of inadequate management of the second relationship: the parents were not adequately informed, the consent they gave was not fully informed, and the legal consequence followed.

The catastrophic injury context. Pediatric malpractice cases that produce permanent injury have damages frameworks distinct from adult cases. The injured child has a lifetime of future care costs, lost earning capacity, and reduced quality of life ahead. Damages in major pediatric malpractice cases routinely run into the millions. In Brown v Meaney, damages were settled prior to trial; the public record does not include the settlement amount but the substantial findings on injury would have supported a major damages settlement.

The treating provider’s continuing relationship. Many pediatric malpractice cases involve a treating provider who continues to see the patient or to be otherwise involved in subsequent care. The relationship adds complexity to the litigation. The legal framework does not require the physician to admit error or to change the ongoing care relationship, but it does require honest communication about the events. The disclosure framework I covered in Communication Failures, Continuity of Care, and Medical Malpractice applies to pediatric cases as well.

Why this case matters

For families of children with developmental disabilities. Many families with children who have severe developmental disabilities live with the question of whether something different in the early clinical course could have produced a better outcome. The question is often unanswerable on the available evidence. Brown v Meaney illustrates the kind of case where the question has a clear legal answer: a recognized clinical syndrome, a clear standard of care, a documented breach, and direct evidence of the counterfactual through a sibling. Where these features are present, a malpractice claim is viable. Where they are not, the case is much more difficult.

For more on the general framework for evaluating these cases, see Suing for Medical Malpractice in Ontario: What You Need to Know and the firm’s Birth Injury practice page.

For pediatric neurologists and clinical teams. A few practical observations:

Document the clinical reasoning, not just the decisions. Where a treatment trial is discontinued or where a recurrence is managed in a particular way, the chart should reflect the reasoning. Subsequent legal analysis turns substantially on what the chart shows. A chart that records only the conclusion is harder to defend than one that records the deliberation.

Communicate the alternatives to families. The informed consent obligation includes alternatives, even alternatives that the clinical team does not propose to use. Where a low-risk alternative exists and is being deferred, the family should know about it and the basis for the deferral.

Reassess when the clinical picture changes. The May 26, 2003 recurrence was a new piece of clinical information that warranted reassessment of the prior decisions. Where a clinical event occurs that is consistent with a particular diagnostic hypothesis, the hypothesis should be revisited explicitly. The chart should reflect that reconsideration.

The “first do no harm” framing is not always neutral. Clinical conservatism (waiting, observing, not intervening) is sometimes the right call. But where a low-risk intervention is available and the alternative is continuing seizures or other recognized harm, the conservative path is not actually the safer path. The trade-off analysis must be calibrated to the actual risks of intervention and non-intervention.

Cluster integration

The plaintiff-success cluster:

• Kotorashvili v Lee (orthopedic, administrative-clinical workflow)
• Henry v Zaitlen (delayed referral)
• Denman v Sabapathy (informed consent)
• Hemmings v Peng (obstetric anaesthetic)
• Hasan v Trillium Health Centre (stroke; Snell framework)
• Gumbley v Vasiliou (asthma intubation delay)
• Dallner v Gladwell (orthopedic brachial plexus injury)
• Brown v Meaney (pediatric PDE)

Eight plaintiff-success cases now anchor the cluster.

The informed consent cluster:

• Denman v Sabapathy (principal Ontario plaintiff anchor)
• Brown v Meaney (pediatric informed consent with low-risk alternative)
• Gilmore v Ferguson (BC plaintiff success)
• Khaleel v Coon (Alberta plaintiff success)
• Noel v Hawrylyshyn (Ontario defendant success)
• A.G. v Rivera (BC defendant success)

The low-risk alternative framework (new for the cluster):

• Brown v Meaney is the principal cluster authority on this framework
• Connects to the broader “common practice” framework from ter Neuzen v Korn

The natural experiment as causation evidence (new for the cluster):

• Brown v Meaney is the principal cluster authority
• Twin sister comparison as direct counterfactual evidence
• Generalizable to any case where a comparable contemporaneous patient is available

The “common practice as defence” framework:

• Ter Neuzen v Korn, [1995] 3 SCR 674 (foundational SCC authority)
• Brown v Meaney (application — common practice fraught with obvious risk)
• Dallner v Gladwell (related application — extreme rarity of complication)

The pediatric / brain injury / developmental disability practice area:

• Brown v Meaney is the principal cluster authority for delayed-treatment pediatric brain injury cases
• Connects to birth injury cluster
• Distinct from intrapartum brain injury (Hemmings, Henry) — addresses post-natal treatment timing

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Decision Date: December 30, 2024

Jurisdiction: Ontario Superior Court of Justice

Citation: Brown v Meaney, 2024 ONSC 7256 (CanLII)

Trial Judge: Justice Michael Bordin

Outcome: Plaintiff trial win on liability. Damages settled prior to trial. The trial judge found that the defendant pediatric neurologists at McMaster Children’s Hospital had breached the standard of care in (a) failing to implement a monotherapy trial before May 20, 2003; (b) failing to maintain an adequate observation period after discontinuing pyridoxine on May 16, 2003; (c) failing to consider restarting pyridoxine when seizures returned on May 26, 2003; and (d) blindly following a common practice that was fraught with obvious risk rather than administering an innocuous vitamin that could have mitigated severe risks without causing harm. The trial judge also found a breach of the duty to obtain informed consent, with the modified objective test satisfied by the mother’s testimony that she would not have consented to discontinuing B6 had she been adequately informed. Causation was established with reference to the regression in the patient’s development after the relevant events, the slowdown in brain growth, and the comparison with her twin sister Summer who received early pyridoxine treatment and had a better neurodevelopmental outcome.

Key authorities: Reibl v Hughes, [1980] 2 SCR 880 (informed consent framework); Hopp v Lepp, [1980] 2 SCR 192 (informed consent); ter Neuzen v Korn, [1995] 3 SCR 674 (common practice as defence; the “fraught with obvious risk” qualifier); Clements v Clements, 2012 SCC 32 (but-for causation); Snell v Farrell, [1990] 2 SCR 311 (robust and pragmatic causation).