Dickinson v Newcastle NHS Trust: Clinical Negligence, Wernicke’s Encephalopathy and Functional Neurological Disorder

The judgment in Dickinson v Newcastle Upon Tyne Hospitals NHS Foundation Trust [2026] EWHC 1574 (KB) is likely to attract close attention from clinical negligence practitioners, neurologists, psychiatrists, neuropsychiatrists and expert witnesses. It concerns an admitted failure to administer prophylactic thiamine, in the form of Pabrinex, to a patient at risk of Wernicke’s encephalopathy, and the subsequent development of disabling functional neurological and cognitive symptoms.

The case is important not simply because of the severity of the claimant’s presentation, but because of the Court’s analysis of causation. The Defendant admitted breach of duty in failing to administer an appropriate course of Pabrinex during an August 2016 admission, when the Claimant was alcohol dependent and being treated with chlordiazepoxide for alcohol withdrawal symptoms. The central issue was whether that breach caused Wernicke’s encephalopathy and, in turn, whether the episode and its psychological consequences caused a functional neurological symptoms disorder, including functional neurological disorder and functional cognitive disorder. The judgment records that the Claimant had developed FND, functional cognitive disorder and depressive disorder, giving rise to profound physical disability and functional cognitive and memory disorder.

For those involved in clinical negligence expert witness work, the judgment provides a useful illustration of the Court’s approach to medical causation where organic pathology, functional symptoms, psychiatric reaction, pre-existing vulnerability and contested expert opinion all interact.

Background to the clinical negligence claim

The Claimant, Liam Dickinson, was admitted to the Freeman Hospital in August 2016 for treatment of a facial lesion. He had a background of chronic alcoholism and was treated with chlordiazepoxide for alcohol withdrawal. It was accepted that he should have received prophylactic thiamine in the form of Pabrinex, and that the failure to administer a proper course amounted to a breach of duty. The judgment records that even the first dose was not properly administered and that no further doses of Pabrinex were given during the admission.

The Claimant’s case was that the failure caused thiamine deficiency, which caused Wernicke’s encephalopathy. He then developed a disabling functional disorder affecting physical and cognitive function, together with major reactive depression. The Defendant did not materially dispute the Claimant’s current condition, but denied causation. Its case was that the symptoms were coincidental or pre-existing, or that they worsened for reasons unrelated to the failure to administer thiamine.

The factual chronology was clinically significant. Before discharge, the Claimant reported feeling “drunk” when outside and needing to sit down. The day after discharge, his wife described him as confused, unsteady, falling over and appearing “brain damaged”. A GP noted confusion, dizziness, sleepiness and mildly ataxic gait, and wondered about Wernicke’s encephalopathy. Later that evening, hospital records documented acute confusion and possible Wernicke’s encephalopathy, with subsequent findings including confusion, balance problems, ataxia and paraesthesia.

This sequence mattered because it provided contemporaneous clinical evidence against which later expert opinions had to be tested. In medico-legal practice, this remains a familiar point: later retrospective analysis is important, but contemporaneous observations by treating clinicians often carry substantial evidential weight.

Wernicke’s encephalopathy and the importance of thiamine

Wernicke’s encephalopathy is a neurological emergency caused by thiamine deficiency. It is classically associated with confusion, ataxia and eye movement abnormalities, although the full triad is not always present. BMJ Best Practice describes Wernicke’s encephalopathy as an acute neurological emergency caused by vitamin B1 deficiency, most commonly associated with poor intake or malabsorption, particularly in chronic alcohol-use disorder; treatment is urgent parenteral thiamine to avoid permanent neurological injury and death. (Best Practice)

NICE guidance on alcohol-use disorders advises clinicians to maintain a high level of suspicion for Wernicke’s encephalopathy and to offer parenteral thiamine to people with suspected Wernicke’s encephalopathy. It further states that parenteral treatment should be given for a minimum of five days unless Wernicke’s encephalopathy is excluded, followed by oral thiamine. (NICE)

In Dickinson, the need for thiamine prophylaxis was not the disputed issue. The significance of the judgment lies in what followed from the admitted omission. The Court concluded, on the balance of probabilities, that the Claimant did develop Wernicke’s encephalopathy on 31 August into 1 September 2016. The Court accepted that it was relatively mild, while expressly recognising the seriousness of the condition, and found that it responded quickly to high-dose intravenous Pabrinex.

That finding was central. Without establishing Wernicke’s encephalopathy, the Claimant’s causation case would have been more difficult. With it, the Court then had to consider whether the organic episode, and the Claimant’s awareness of its implications, formed the causal route to the later functional disorder.

Functional neurological disorder in a medico-legal context

Functional neurological disorder, sometimes referred to in broader terms as functional neurological symptoms disorder, can cause severe physical and cognitive disability. It is not synonymous with fabrication, malingering or symptoms that are “all in the mind”. Nor should it be treated as a diagnosis of exclusion.

NICE Clinical Knowledge Summaries states that FND should be a “rule-in” diagnosis, made by identifying positive signs of FND in association with symptoms consistent with the disorder. Positive signs include internal inconsistency or signs incongruent with recognised neuroanatomical pathways. NICE further states that FND should not be a diagnosis of exclusion. (CKS)

This is highly relevant in litigation. FND claims can be vulnerable to oversimplification. Defendants may argue that symptoms are pre-existing, disproportionate, psychologically mediated, unrelated to the index event, or not caused by breach. Claimants may argue that an accident, medical event, diagnostic experience or psychological stressor caused or materially contributed to the onset of functional symptoms. The task for the Court is not to decide whether symptoms are “organic” or “psychological” in a crude binary sense, but to consider the evidence as a whole.

In Dickinson, the Court accepted that the Claimant’s functional disorder had its genesis in the significant psychological stressor of discovering that he had developed a serious neurological disorder, with potentially grave and permanent consequences, by reason of the failure to administer appropriate Pabrinex.

That finding is clinically and legally important. The Court did not require the functional disorder to be caused by continuing structural neurological damage. Rather, it accepted a causal pathway in which an organic episode of Wernicke’s encephalopathy and the Claimant’s awareness of its significance precipitated a disabling functional condition.

The expert evidence

The judgment illustrates the importance of carefully reasoned expert evidence in complex causation cases. The Court considered evidence from a range of disciplines, including neurology, neuropsychiatry, psychiatry and care experts. The parties disputed whether Wernicke’s encephalopathy had occurred, whether functional symptoms were pre-existing, and whether the admitted breach was causative.

One of the notable aspects of the judgment is the Court’s engagement with contemporaneous records. The Court criticised expert reasoning that retrospectively discounted the conclusions of treating clinicians. It found the attitude of some defence expert evidence to contemporaneous notes and treating clinicians’ conclusions unconvincing, observing that there appeared to be excessive confidence in retrospectively second-guessing those clinicians.

This is a useful reminder for expert witnesses. In medico-legal reporting, the expert’s task is not to construct a theoretical explanation detached from the clinical chronology. A persuasive report should address the records directly, identify the significance of contemporaneous findings, explain apparent inconsistencies, and avoid overreaching beyond the expert’s discipline.

The case also demonstrates the importance of multi-disciplinary understanding. Wernicke’s encephalopathy is a neurological emergency. FND sits at the interface of neurology, psychiatry, psychology and rehabilitation. Depression, alcohol dependence, chronic pain and pre-existing psychiatric vulnerability may all be relevant to prognosis and quantum, but they do not necessarily defeat causation if the index breach is shown to have caused the material injury on the balance of probabilities.

Causation: the legal framework

The Court approached causation by applying orthodox principles. Given the admission of breach of duty, the issue was whether the Claimant had proved causation on the balance of probabilities. The judgment records that the causation question was to be resolved by considering expert opinions, contemporaneous records and witness evidence.

The Court referred to the standard “but for” test in Bolitho v City and Hackney Health Authority, namely that where breach is proved or admitted, the claimant must still prove that the breach caused the injury. It also referred to Clerk & Lindsell’s formulation: would the damage have occurred but for the defendant’s negligence? If the damage would have occurred in any event, the defendant’s conduct is not a “but for” cause.

The Court did not need to decide the case by applying material contribution principles. This is significant. Dickinson was not treated as a case in which the claimant succeeded merely because the breach made some contribution to an indivisible injury. The Court found that, but for the admitted breach, the Claimant would not have developed the functional disorder.

The key conclusion was expressed clearly: the episode of Wernicke’s encephalopathy and its effect on the Claimant caused the functional neurological symptoms disorder on the balance of probabilities. The timing was not merely coincidental, nor simply a milestone in an inevitable deterioration. Liability was therefore established.

Why the judgment matters for clinical negligence practitioners

Dickinson is likely to be cited in future cases involving FND, functional cognitive disorder, Wernicke’s encephalopathy, alcohol withdrawal management, Pabrinex administration and disputed clinical negligence causation. Its importance lies in several practical points.

First, the judgment reinforces the need for careful risk management in patients with alcohol dependence. Failure to administer parenteral thiamine to an at-risk patient may have serious neurological consequences. For clinicians and NHS Trusts, documentation of prescribing, administration and missed doses remains essential.

Secondly, the case shows that FND can form part of a successful clinical negligence claim where the evidential chain is properly established. It is not enough for a defendant to characterise symptoms as functional and then assume causation fails. Functional disorders can be disabling, clinically recognised and causally linked to an index medical event or negligent omission.

Thirdly, the judgment demonstrates the significance of psychological stressors in FND causation. In this case, the Claimant’s awareness that he had developed a serious neurological condition, probably caused by the failure to provide appropriate Pabrinex, was central to the Court’s reasoning. That does not mean that every diagnosis, medical complication or adverse clinical experience will cause FND. It does mean that the Court will examine whether a plausible and evidence-based causal mechanism exists.

Fourthly, the case underlines the forensic value of contemporaneous medical records. The sequence of confusion, ataxia, concern about Wernicke’s encephalopathy and response to intravenous Pabrinex was not merely background detail. It was central to the Court’s finding that Wernicke’s encephalopathy had occurred and that the later functional disorder was not simply pre-existing.

Implications for expert witnesses

For expert witnesses, Dickinson provides several lessons. Reports in similar cases should identify the relevant standard of care, but where breach is admitted, the report must focus with particular discipline on causation. The expert should set out the competing causal hypotheses, assess the chronology, address pre-existing vulnerabilities, and explain why the index event did or did not make the decisive difference.

In FND cases, experts should be cautious about language. FND is not a diagnosis of exclusion and should not be treated as a proxy for exaggeration. A proper opinion should consider positive clinical signs, consistency with recognised diagnostic criteria, the role of psychological stressors, the timing of onset, comorbid psychiatric conditions and the distinction between vulnerability and causation.

In Wernicke’s encephalopathy cases, expert evidence should consider the patient’s nutritional state, alcohol history, presenting symptoms, timing of thiamine administration, response to treatment and the extent to which later symptoms are attributable to organic injury, functional disorder, psychiatric reaction or a combination of these.

The judgment is also a reminder that courts are alert to hindsight reasoning. An expert who gives insufficient weight to treating clinicians’ records, or who retrospectively dismisses contemporaneous diagnoses without adequate explanation, may be less persuasive.

Conclusion

Dickinson v Newcastle Upon Tyne Hospitals NHS Foundation Trust [2026] EWHC 1574 (KB) is a significant clinical negligence judgment on causation, Wernicke’s encephalopathy and functional neurological disorder. It confirms that a claimant may succeed where an admitted breach caused an acute neurological episode, and where the consequences of that episode, including the claimant’s psychological response to it, caused disabling functional symptoms.

The case does not create a special rule for FND claims. Rather, it applies orthodox causation principles to complex medical facts. Its value lies in the Court’s careful analysis of the clinical chronology, expert evidence and competing explanations. For solicitors, barristers and expert witnesses, it is a useful example of how causation may be established in cases where the boundary between neurological injury, psychiatric response and functional symptoms is clinically complex but legally determinable.

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