Cauda equina syndrome (CES) is the spinal cord emergency most frequently litigated in UK practice — the cauda equina is the collection of L2-S5 nerve roots in the lumbar spinal canal below the conus medullaris (typically at L1-L2 level). Compression of these roots (most commonly by a massive L4/5 or L5/S1 disc prolapse, but also by tumour, haematoma, or abscess) causes the CES syndrome. The cardinal features are: bladder dysfunction (urinary retention — inability to void, or urinary incontinence from overflow retention), bowel dysfunction (faecal incontinence or constipation), saddle anaesthesia (numbness/reduced sensation in the perineum, buttocks, and inner thighs — the distribution of nerves that contact a saddle), and bilateral lower limb weakness and/or sciatica. The medicolegal risk: a GP who sends a patient with back pain + urinary symptoms home without specifically asking about saddle anaesthesia and arranging urgent MRI has potentially missed CES. The standard of care: any patient with back pain + any of: urinary retention or altered urinary sensation, saddle anaesthesia, bilateral sciatica or progressive leg weakness requires immediate emergency assessment and urgent MRI via the local spinal pathway. Urinary retention is particularly concerning; incontinence may be a late feature.

The Babinski sign (upgoing plantar response) is the most important single clinical sign distinguishing upper from lower motor neurone pathology — it is elicited by slowly stroking the lateral sole of the foot from heel to ball with a blunt object (tongue depressor, key, or end of patella hammer). A normal adult response is plantar flexion of the great toe (downgoing) with or without flexion of the other toes. An upgoing plantar (Babinski positive) consists of dorsiflexion (extension) of the great toe with fanning of the other toes — this indicates damage to the corticospinal tract (UMN pathway) from any level between the motor cortex and the spinal cord segment supplying the foot. A positive Babinski in an adult with leg weakness = UMN pathology — localise clinically and arrange imaging via the appropriate urgent pathway depending on associated signs. The caveats: Babinski is normally present in infants under approximately 18 months (immature corticospinal tracts); it may be difficult to elicit in patients with significant foot pain, severe peripheral neuropathy, or very anxious patients; a true positive requires the specific toe extension pattern, not just general withdrawal from tickling.

The MRC muscle strength grading scale (0-5) is the standard clinical tool for documenting motor weakness and tracking progression over time — it is essential for both diagnosis and medicolegal documentation: Grade 0 = No visible or palpable contraction; Grade 1 = Visible or palpable contraction but no movement; Grade 2 = Movement with gravity eliminated (horizontally); Grade 3 = Movement against gravity only (cannot resist any additional force); Grade 4 = Movement against gravity and some resistance (4- = minimal resistance, 4 = moderate, 4+ = good resistance); Grade 5 = Normal strength. In practice, most clinically significant weakness producing functional impairment will be grade 3-4. The distinction between grade 4 and grade 5 requires consistent application — a patient with MRC 4/5 hip flexion bilaterally who had previously normal strength has a significant finding that requires explanation. Documenting 'power normal' without specifying muscle groups and MRC grade is inadequate neurological documentation.

Foot drop (failure to dorsiflex the foot and toes — L4/L5 innervation via the common peroneal nerve) is one of the most common monosymptomatic presentations of leg weakness in primary care, and accurate localisation of the lesion is critical for correct management. The three anatomical sites causing foot drop that every GP must distinguish: (1) Peroneal nerve palsy at the fibular head (most common, from prolonged leg crossing, weight loss, casting, fibular fracture, or prolonged squatting): foot drop with no knee extension weakness, sensory loss over dorsum of foot + lateral calf, no reflex change — this is an LMN peripheral nerve lesion that often recovers spontaneously with removal of the compressive cause; (2) L5 radiculopathy (L4/5 disc prolapse): foot drop with sciatica (radiating to big toe), no ankle reflex change, positive SLR — MRI only if red flags/progressive deficit or the result is likely to change management; (3) Cortical or corticospinal stroke (foot drop as part of hemiplegia): UMN signs, spasticity, hyperreflexia, upgoing plantar, associated arm weakness — requires the stroke pathway. A GP who applies a foot drop brace without localising the anatomical cause has not adequately assessed the patient.

Malignant spinal cord compression (MSCC) is one of the most time-critical oncological emergencies and one that GPs can prevent or minimise disability from by proactive action. The tumours most commonly responsible: lung (most common), breast, prostate, myeloma, kidney, colorectal. The clinical warning signs (PREMONITORY) that occur days to weeks before complete cord compression: back pain (the most common symptom — localised, constant, worse lying down at night, unlike mechanical back pain); progressive lower limb weakness; altered sensation in the legs; urinary frequency or retention. A cancer patient presenting with new back pain that is different from previous pain (constant, nocturnal, worsening) should trigger urgent MSCC assessment: contact the MSCC coordinator, dexamethasone 16 mg as soon as possible if neurological signs/symptoms, and whole-spine MRI as soon as possible and always within 24 hours. NICE NG234 (spinal metastases and MSCC, 2023) is explicit: suspected MSCC with neurological symptoms or signs = dexamethasone 16 mg without delay, whole-spine MRI as soon as possible and always within 24 hours, and early contact with the MSCC coordinator.

The IVIG vs plasmapheresis equivalence in Guillain-Barré syndrome is established by multiple RCTs and systematic reviews — both treatments are equally effective at reducing disability and time to recovery in moderate-severe GBS (defined as inability to walk unaided). The choice is made based on availability, local expertise, and patient factors: IVIG (intravenous immunoglobulin 0.4 g/kg/day for 5 days) is more widely available, easier to administer, and equally effective. Plasmapheresis (plasma exchange — typically 4–5 exchanges over 1–2 weeks) requires a specialised centre and venous access. The critical principle: combination therapy (IVIG + plasmapheresis together) is NOT more effective than either alone. Steroids are CONTRAINDICATED in GBS — multiple RCTs show that steroids do not improve outcomes and may prolong the disease. This is one of the most important exceptions to the general principle of treating inflammatory neurological conditions with corticosteroids. GPs presenting a suspected GBS patient to the medical team should specifically mention 'no steroids for GBS.'

Dermatomyositis (proximal myopathy + heliotrope rash + Gottron's papules + raised CK) is associated with underlying malignancy, which may precede, coincide with or follow the diagnosis. Malignancy assessment should be specialist-led and tailored to age, sex and clinical phenotype; GPs should ensure referral is urgent and that any specialist-recommended surveillance is completed and documented.

Driving advice for leg weakness should follow the current DVLA "Assessing fitness to drive" standards for the specific diagnosis (for example stroke, cauda equina syndrome, MS or MND), which differ between Group 1 and Group 2 licences and are updated periodically — check the current chapter rather than relying on fixed intervals. The GP's responsibilities: (1) advise the patient whether they must stop driving and whether they need to notify the DVLA (the licence holder's legal duty); (2) document this advice in the clinical record; (3) if a patient continues to drive against advice where there is a serious road-safety risk, GMC confidentiality guidance allows the doctor to inform the DVLA, telling the patient first. Driving assessment centres (approved by DVLA) can assess adapted vehicle control for patients who wish to continue driving with adaptations.

The dermatomyositis associated malignancy and the MSCC dexamethasone immediate prescription are two of the most important and high-stakes actionable clinical decisions in the management of leg weakness — they both illustrate that leg weakness is not just a rehabilitation challenge but a diagnostic investigation pathway with life-changing implications. GPs who approach leg weakness with a structured anatomical framework (UMN vs LMN, spinal vs peripheral, proximal vs distal), a systematic examination (tone, power, reflexes, sensation, coordination, plantars), and a low threshold for urgent assessment and targeted imaging in new progressive weakness, will identify the serious and treatable causes before permanent neurological damage occurs. The single most important clinical principle in leg weakness: any progressive leg weakness without a clear established cause needs urgent investigation — 'watchful waiting' is not appropriate for new progressive neurological weakness.