Abstract

Neurological symptoms are common across primary care, acute medicine and same-day emergency care (SDEC), yet they can be difficult to triage confidently.

On 13 February 2026, the University of Liverpool’s Brain Infection and Inflammation Group hosted NeuroPRACTICE, a practical course aimed primarily at local general practitioners and non-neurology specialists. This report highlights key learning points from the day: defining true thunderclap headache, distinguishing migraine from secondary headache disorders, understanding the growing role of CGRP antagonists, recognising TIA and stroke mimics, approaching back pain through biomechanical and pain-mechanism frameworks and using patient-centred language to explain functional neurological disorder. The course successfully translated specialist neurology into pragmatic, clinically useful tools for non-specialists.

Introduction

On 13 February 2026, I had the pleasure of attending the NeuroPRACTICE course hosted by the University of Liverpool’s Brain Infection and Inflammation Group. Although the course was aimed mainly at general practitioners in the region, I attended as an internal medicine doctor and found it highly relevant to acute medical practice.

Many of the same patients discussed during the day are those we see on the acute take, in same-day emergency care and on the wards: people with severe headache, transient neurological symptoms, dizziness, collapse, back pain, tremor, dissociative seizures or symptoms that do not fit neatly into a single speciality pathway.

From the outset, the day was exceptionally well run. The welcoming atmosphere, excellent refreshments and generous lunch created an ideal setting for learning. More importantly, the course allowed attendees to ask practical questions of leading specialists and to think collaboratively about how patients move between primary care, acute medicine, emergency medicine and neurology.

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The strength of the day lay not only in clinical updates, but in the language and frameworks it gave us. I left with clearer ways to describe migraine, thunderclap headache, TIA mimics and functional neurological disorder – not just to colleagues, but to patients and families.

1. Migraine, thunderclap headache and the new CGRP landscape

Dr Viraj Bharambe’s session on migraine was one of the most immediately useful parts of the course. His key phrase – ‘Migraine is not a headache; it is a process’ – reframed a diagnosis that is often oversimplified in both primary and acute care [1].

This distinction matters because migraine may include prodrome, aura, sensory symptoms, nausea, photophobia, cognitive slowing and postdromal fatigue. Explaining this breadth of neurological symptoms to patients can reduce anxiety, particularly when aura, sensory disturbance or cognitive slowing are mistaken for signs of a more sinister acute disorder.

The most helpful part of the session was the discussion around thunderclap headache. As an internal medicine doctor, I frequently see patients referred with ‘thunderclap headache’ because of understandable concern about subarachnoid haemorrhage. In practice, many of these histories become less typical for SAH once explored carefully: the headache may have built over 30–60 minutes, occurred in the context of a migraine phenotype, or been described as ‘the worst headache’ rather than truly maximal at onset.

The course clarified an important clinical maxim: ‘Thunderclap headache is a temporal diagnosis, not just a severity diagnosis.’ NICE defines thunderclap headache as a sudden severe headache typically peaking within 1–5 minutes and advises that it should prompt consideration of SAH while also recognising that most thunderclap headaches are not ultimately due to SAH [2].

This matters because once the label ‘thunderclap’ is applied, patients may enter a high-anxiety and resource-intensive pathway involving CT brain imaging, lumbar puncture and prolonged observation. The learning point was not to become complacent about SAH, but to ask better questions: How quickly did the headache reach maximum intensity? Was it instant, within seconds to minutes, or did it build? Was there collapse, vomiting, meningism, exertional onset, pregnancy or postpartum context, anticoagulation, immunosuppression or neurological deficit?

The evidence supports this nuance. In the international HEAD study, 644 of 4,536 emergency department headache presentations were classified as thunderclap headache; serious pathology was found in 10.9%, SAH in 3.6% and all SAH cases were diagnosed on CT imaging [3]. The more recent UK SHED study found that after a negative CT performed within six hours of onset, the post-test probability of SAH was 0.5%, supporting shared decision-making about further investigation in selected patients [4]. Lumbar puncture remains important where suspicion persists, but studies of CT-negative headache pathways demonstrate low diagnostic yield in low-risk groups, alongside complications such as traumatic taps, post-lumbar puncture headache and prolonged emergency department stay [5,6].

Once acute secondary causes such as SAH are confidently excluded, the clinical focus must shift to optimising primary headache management to prevent recurrent hospital attendances. This brings us to the second major update from the session: the growing role of gepants.

Rimegepant and atogepant are oral CGRP-pathway drugs that have recently entered prescribing conversations. This felt especially timely from my perspective as a clinician working in Liverpool, because the Cheshire and Merseyside formulary now includes rimegepant for both prevention and acute treatment of migraine in line with NICE TA906 and TA919, while atogepant has been approved locally for prevention in line with NICE TA973 [7–10]. NICE has also reported rapid primary-care uptake of atogepant and rimegepant in England following approval [11].

The science behind this is elegant. CGRP is central to trigeminovascular signalling in migraine and CGRP-targeted therapies represent a successful translation of molecular neuroscience into clinical practice [12]. For GPs and acute physicians, the key is to document migraine days, headache days, disability, medication-overuse risk, previous preventives, contraindications and response to treatment. This makes referral more efficient and helps identify patients who may meet criteria for newer therapies.

2. TIA, stroke mimics and the value of negative symptoms

Dr John Williamson’s session on transient neurological symptoms was highly practical [13]. This was another area that translated directly into acute medical work. Patients with possible TIA or stroke mimics often arrive via multiple routes: GP, emergency department, SDEC, paramedics or self-presentation.

The course provided a simple but powerful framework: ‘True TIA and stroke symptoms are usually focal, negative and maximal at onset.’

Negative symptoms include loss of power, loss of sensation, loss of speech or loss of vision. By contrast, migraine aura often begins with positive symptoms – flashing lights, zig-zag lines, tingling or spreading sensory disturbance – and evolves gradually over minutes. Seizure, syncope, vestibular syndromes, hypoglycaemia and functional symptoms can also mimic cerebrovascular events [14,15].

One of the most useful practical questions from the day was: ‘What did the patient lose?’ A patient with sudden-onset right arm weakness and expressive dysphasia for 15 minutes is different from a patient with tingling that spreads from hand to face over 20 minutes followed by headache. Both deserve careful assessment, but they do not carry the same pre-test probability of TIA.

The session did not encourage clinicians to downgrade risk. Rather, it encouraged better characterisation. A referral that clearly describes time course, symptom type, vascular risk factors, associated headache, loss of consciousness, witnessed events and recovery pattern is far more useful than a generic ‘?TIA’. This is where primary and secondary care can genuinely improve the patient pathway.

3. Back pain: pain mechanisms, spinal stability and risk stratification

Mr Nick Carleton-Bland’s session on back pain addressed one of the most common and burdensome presentations in both primary care and acute medicine [16]. Low back pain remains the leading global cause of years lived with disability, affecting an estimated 619 million people in 2020, with projections of 843 million by 2050 [17].

The session’s classification of pain into nociceptive, neuropathic and nociplastic categories was particularly useful. It allowed back pain to be discussed not just anatomically, but mechanistically. This aligns with modern pain medicine and with NICE guidance, which recommends assessing for serious pathology, avoiding routine imaging in non-specialist settings, encouraging self-management and normal activity and using risk stratification to identify patients at higher risk of poor outcome [18].

The session also reframed spinal stability through Panjabi’s model, which describes three interacting subsystems: the passive subsystem of vertebrae, discs and ligaments; the active subsystem of muscles and tendons; and the neural-control subsystem that coordinates movement and stability [19]. This was a helpful way of explaining why conservative management and physiotherapy matter. For the majority of patients with non-specific low back pain, treatment is not simply about ‘finding the damaged structure;’ it is about restoring confidence, movement, muscular support and control.

The practical message was that most acute lower back pain is non-specific and self-limiting, but clinicians must remain alert to red-flag features such as bladder or bowel disturbance, saddle anaesthesia, major trauma, constitutional symptoms, fever, immunosuppression, history of malignancy, inflammatory features or progressive neurological deficit, which may indicate cauda equina syndrome, fracture, malignancy, infection or inflammatory disease. For acute and primary care, the challenge is to provide reassurance without minimising symptoms and safety-netting without over-medicalising pain.

4. Movement disorders and explaining FND well

Dr Michael Bonello offered a clear, axis-based approach to movement disorders, separating hypokinetic syndromes such as Parkinson’s disease from hyperkinetic presentations such as tremor, dystonia, chorea and myoclonus [20]. This made movement phenomenology feel more manageable for non-neurologists.

The discussion of Parkinson’s disease was useful for community and ward-based practice. Wearing-off, delayed ‘on’ periods, dyskinesia and non-motor fluctuations should be actively sought. NICE emphasises patient-centred communication, specialist review, Parkinson’s nurse involvement and caution before altering complex dopaminergic regimens without specialist advice [21].

The most personally useful part of this section, however, was the discussion around functional neurological disorder and dissociative seizures. In acute medicine, we often meet patients and families at a moment of fear and frustration. They may have been told tests are normal, or that symptoms are ‘not epilepsy’ or ‘not stroke’, but without being given a positive explanation for what the symptoms are.

The course provided vocabulary that felt much more patient-centred. FND symptoms are real, involuntary and potentially treatable. They are not imagined, faked or ‘all in the mind’. Current models understand FND as a disorder of brain network function, involving altered attention, prediction, motor control, emotion processing and sense of agency [22–24]. Recent practical guidance emphasises that FND should be diagnosed using positive clinical features, not simply by exclusion and that clear explanation is an important part of treatment [25].

This matters on the ward and in SDEC. A helpful explanation might be: ‘Your nervous system is not damaged, but it is not functioning normally at the moment – a bit like a software problem rather than a hardware problem. The symptoms are real and the good news is that function can improve with the right strategies.’

For families, this language can be transformative. It validates the patient’s experience while opening the door to rehabilitation, grounding techniques, physiotherapy, psychology and self-management.

The course also introduced practical strategies such as sensory grounding, controlled breathing and progressive muscle relaxation [26,27]. These techniques are not merely ‘psychological’. They have a physiological rationale. Patients with functional seizures or other FND symptoms may enter a heightened ‘red alert’ state, with autonomic arousal and sometimes hidden hyperventilation. Slow breathing techniques, such as 4–8 breathing, may help stabilise ventilation and carbon dioxide balance, reducing dizziness, tingling, chest tightness and panic-like bodily sensations that can perpetuate the cycle [28]. Sensory grounding similarly redirects attention from threat monitoring towards present-moment sensory cues, helping the patient regain a sense of control.

I would avoid overstating this as ‘rewiring the brain’ in a literal sense, but it is reasonable to describe these tools as ways of reducing arousal, attentional capture and symptom-related threat responses while patients await specialist input.

5. Educational innovation: making learning last

Beyond the clinical content, the course team described an AI-supported learning tool designed to help attendees consolidate learning after the event. This was a forward-thinking addition. A single study day can be inspiring, but knowledge decays quickly unless revisited.

The educational rationale is strong. Spaced repetition and retrieval practice are among the most robust findings in cognitive psychology and spaced digital education has been shown to improve knowledge, skills and, in some settings, clinical behaviour among health professionals [29,30]. Adaptive learning systems may be particularly useful in neurology education because much of the skill lies in repeated pattern recognition: thunderclap headache versus migraine, TIA versus aura, epileptic versus dissociative seizures and Parkinsonian tremor versus essential tremor.

If developed with transparent sourcing, clinician oversight and appropriate evaluation, such tools could help convert a one-day course into durable practice change.

Conclusion

The Liverpool NeuroPRACTICE course achieved what many clinical education events aim for but do not always deliver: it made neurology feel usable. Although primarily aimed at local GPs, it was highly relevant to my work as an internal medicine doctor seeing patients on the acute take, in SDEC and on the wards.

The most valuable lessons were practical and patient-facing. I left better able to define true thunderclap headache, separate migraine biology from SAH red flags, recognise that TIA and stroke usually produce negative symptoms and explain FND in language that validates patients and helps families understand the diagnosis. The update on gepants was also timely, particularly given their appearance in regional prescribing pathways.

Overall, NeuroPRACTICE successfully familiarised non-specialists with common neurological presentations, strengthened the primary-secondary care interface and provided a pragmatic model for neurology education in the modern NHS.

References

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