PACES neurology station: why it costs the most marks and how to prepare
Neurology showed the largest gap from the maximum score of any PACES encounter in 2025. A localisation-first approach, the clinching signs and the common cord, brain, nerve and muscle cases.
The short answer
- Neurology is the second half of Station 3: up to 6 minutes to examine, then at least 4 minutes of questions. The examiner will point you to the part of the body to examine.
- In the Federation’s 2025 report, neurology showed the largest gap between candidates’ average score and the maximum of any PACES encounter.
- The fix is a localisation-first approach: decide where the lesion is (upper or lower motor neurone, cord, cerebellum, basal ganglia, nerve, junction or muscle) before what it is.
- Look for the clinching sign: tongue fasciculations (MND), fatigability (myasthenia), cape-like loss of pain and temperature (syringomyelia), brisk knees with absent ankle jerks (B12 deficiency), preserved inversion in foot drop (common peroneal palsy).
Why neurology costs the most marks
Neurology covers a wide range of cases, it depends heavily on technique (tone, reflexes, sensation, coordination), and many candidates find it hard to turn a list of signs into a diagnosis in the time available. The 2025 data reflects that: neurology showed the largest shortfall from the maximum score of any encounter. It is also where a clear, structured approach makes the biggest difference.
Localise first, then find the cause
| Pattern of signs | Where the lesion is | Examples |
|---|---|---|
| Increased tone, pyramidal weakness, brisk reflexes, upgoing plantars, clonus | Upper motor neurone (brain or spinal cord) | Stroke, multiple sclerosis, cord compression, cervical myelopathy, hereditary spastic paraparesis |
| UMN signs below a sensory level, LMN signs at that level | Spinal cord | Cord compression, cervical myelopathy, syringomyelia |
| Wasting, fasciculation, reduced tone, reduced or absent reflexes | Lower motor neurone (anterior horn cell, root, plexus or nerve) | Radiculopathy, peripheral neuropathy, old polio, motor neurone disease |
| Upper and lower motor neurone signs together | Several levels | Motor neurone disease, cervical myelopathy, subacute combined degeneration, Friedreich's ataxia |
| Distal "glove and stocking" sensory loss, reduced ankle reflexes | Peripheral nerves | Diabetic, alcohol-related, drug-induced or B12-related neuropathy; Charcot–Marie–Tooth disease |
| Fatigable weakness and ptosis, normal reflexes and sensation | Neuromuscular junction | Myasthenia gravis |
| Proximal weakness, normal reflexes and sensation | Muscle | Inflammatory, endocrine or drug-induced myopathy; muscular dystrophies |
| Intention tremor, past-pointing, dysdiadochokinesia, nystagmus, ataxic gait, dysarthria | Cerebellum (unilateral signs point to the same side) | Multiple sclerosis, stroke, space-occupying lesion, alcohol, drugs |
| Bradykinesia, rigidity, resting tremor | Basal ganglia | Parkinson's disease, drug-induced parkinsonism, Parkinson-plus syndromes |
Common cases: spinal cord, brain and movement
| Case | Key signs | Points to raise |
|---|---|---|
| Spastic paraparesis | Bilateral UMN signs in the legs, sometimes a sensory level | Differentials: cord compression, cervical myelopathy, multiple sclerosis, B12 deficiency, hereditary spastic paraparesis, cerebral palsy. Urgent MRI if compression is possible |
| Cervical myelopathy | Clumsy hands plus a spastic gait; brisk reflexes, Hoffmann sign, finger escape sign; LMN signs in the arms at the level of compression | MRI cervical spine; spinal surgical assessment if progressive |
| Syringomyelia | Wasted hands (LMN), spastic legs (UMN) and cape-like loss of pain and temperature with preserved vibration and joint position sense | Look for Chiari malformation; MRI of brain and whole spine |
| Subacute combined degeneration | Spastic legs with brisk knee jerks but absent ankle jerks, loss of vibration and joint position sense, positive Romberg | B12 replacement without delay; consider copper deficiency and nitrous oxide use |
| Friedreich's ataxia | Cerebellar and sensory ataxia, areflexia with upgoing plantars, pes cavus, scoliosis | Cardiomyopathy and diabetes; genetic counselling (autosomal recessive) |
| Multiple sclerosis | Signs scattered across the nervous system: pyramidal, cerebellar, internuclear ophthalmoplegia, optic atrophy or RAPD, sensory | Dissemination in space and time; MRI, CSF oligoclonal bands, disease-modifying therapy |
| Stroke (hemiparesis) | Unilateral UMN weakness with lower-face weakness sparing the forehead; aphasia, neglect or a field defect localise the territory | Secondary prevention: antithrombotics, AF, carotids, blood pressure, lipids; rehabilitation |
| Cerebellar syndrome | Intention tremor, past-pointing, dysdiadochokinesia, heel–shin ataxia, nystagmus, broad-based gait | Side of the lesion; causes including MS, stroke, tumour, alcohol and phenytoin |
| Parkinson's disease | Asymmetrical rest tremor, bradykinesia with decrement, rigidity, hypomimia, shuffling gait | Parkinson-plus clues: early falls and vertical gaze palsy (PSP), early autonomic failure (MSA), striking asymmetry and apraxia (corticobasal) |
Common cases: nerve, junction and muscle
| Case | Key signs | Points to raise |
|---|---|---|
| Peripheral neuropathy | Glove and stocking sensory loss, reduced ankle reflexes, sometimes distal weakness and a high-stepping gait | Causes: diabetes, alcohol, B12, drugs (for example chemotherapy, amiodarone), kidney disease, hypothyroidism, paraprotein. Look for a glucose sensor or foot ulcers |
| Charcot–Marie–Tooth disease | Pes cavus, distal wasting ("inverted champagne bottle"), foot drop, areflexia, family history | Inherited; genetic counselling |
| Foot drop | Weak dorsiflexion and eversion | Preserved inversion points to common peroneal palsy (check the fibular neck); weak inversion and hip abduction point to an L5 root lesion |
| Motor neurone disease | Asymmetrical wasting, fasciculation (especially of the tongue), mixed UMN and LMN signs, normal sensation | Riluzole, non-invasive ventilation, nutrition (gastrostomy), multidisciplinary care |
| Myasthenia gravis | Fatigable ptosis and diplopia, fatigable bulbar and proximal weakness; demonstrate it with sustained upgaze, repeated shoulder abduction or counting to 50 | Acetylcholine receptor antibodies, CT thorax for thymoma, FVC monitoring, pyridostigmine; look for a sternotomy (thymectomy) |
| Myotonic dystrophy | Frontal balding, ptosis, temporal wasting, distal weakness, grip and percussion myotonia | Multisystem: cardiac conduction, cataracts, diabetes, sleep and respiratory problems; autosomal dominant |
| Facioscapulohumeral dystrophy | Facial weakness with asymmetrical scapular winging; Beevor's sign | Asymmetry is characteristic |
| Myopathy | Symmetrical proximal weakness, waddling gait, Gowers' sign, normal reflexes and sensation | Look for the cause: thyroid scar, steroids, statins, inflammatory disease |
| Cranial nerve lesions | For example a third nerve palsy, a lower versus upper motor neurone facial palsy, an internuclear ophthalmoplegia, a visual field defect | A pupil-involving third nerve palsy needs urgent vascular imaging; forehead sparing means an UMN facial palsy |
Technique inside 6 minutes
- Listen to exactly what you're asked to examine ("this patient's lower limbs") and stick to it.
- Limbs: inspect (wasting, fasciculation, pes cavus, scars), then tone, power (MRC grading), reflexes (use reinforcement), plantars, coordination and sensation. Offer to examine gait.
- Test sensation to answer a question: is it a dermatome, a peripheral nerve, a glove and stocking pattern or a sensory level?
- Keep moving. A complete, fluent routine scores better than a perfect but unfinished one.
Presenting a neurology case
"This patient has a spastic paraparesis. There is increased tone and pyramidal weakness in both legs, with brisk reflexes, sustained ankle clonus and upgoing plantars, and a sensory level at about T10. This localises to a thoracic spinal cord lesion. The most likely causes are multiple sclerosis or cord compression. I would want to know about bladder and bowel symptoms and arrange an urgent MRI of the spine."
Pattern, then location, then cause, then what you'd do. See how to present a case for more examples.
Sources
Frequently asked questions
What is the hardest station in PACES?
In the Federation’s 2025 PACES report, the neurology encounter showed the largest gap between candidates’ average score and the maximum score of any encounter.
What are the common neurology cases in PACES?
Spastic paraparesis, cervical myelopathy, peripheral neuropathy, Charcot–Marie–Tooth disease, foot drop, Parkinson’s disease, cerebellar syndrome, stroke, multiple sclerosis, motor neurone disease, myasthenia gravis, myotonic dystrophy, myopathy, syringomyelia, Friedreich’s ataxia and cranial nerve lesions.
How do you approach the PACES neurology station?
Examine the part of the body you are directed to, then localise first (upper or lower motor neurone, cord, cerebellum, basal ganglia, nerve, neuromuscular junction or muscle) before suggesting causes and investigations.
How do you tell common peroneal palsy from an L5 radiculopathy?
Both cause foot drop. Ankle inversion is preserved in common peroneal palsy but often weak in L5 radiculopathy, and hip abduction weakness also points to an L5 root lesion.
How long is the PACES neurology examination?
Up to 6 minutes of examination, followed by at least 4 minutes of questions. It follows the cardiovascular encounter at Station 3, unless you are told the order is reversed.
Written by The Ace PACES team. Exam facts are taken from the Federation of the Royal Colleges of Physicians’ published PACES guidance, linked in the sources above. This guide supports exam preparation and is not a clinical guideline.
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