MRCP PACES Peripheral Neuropathy Station: Make Sure You’re Prepared For A Common Case
Here is the blog post:By Dr Will Bierrum, Neurology Registrar and Founder of Medxstart — the success platform for modern doctors, covering medical education, exams, interviews, technology, and ventures beyond medicine.
Peripheral neuropathy is one of the most common neurology stations in MRCP PACES. Most candidates who sit in front of it know the conditions. They have revised the causes of polyneuropathy, they know what Charcot Marie Tooth is and they have read about mononeuritis multiplex. What they need next is a systematic framework to work through the findings under exam pressure.
This post gives you that framework with some key questions to ask yourself in a neuropathy case.
The Five Questions
Before you touch the patient, you need five questions running in the back of your mind.
Are the signs upper motor neurone, lower motor neurone or both?
Is the weakness symmetrical or asymmetrical?
Is it distal, proximal or both?
Is there sensory involvement and if so what type?
Are there any additional cerebellar, pyramidal or extrapyramidal features?
These 5 questions help you work out the clinical syndrome, from there you can apply your knowledge.
Start Before You Examine
The best candidates in PACES have a working hypothesis before they touch the patient. The bedside gives you more information than most people realise if you know what to look for.
Look at the feet and legs first. Ankle foot orthoses or walking aids suggest foot drop. Pes cavus and clawed toes point towards a longstanding or hereditary process. Inverted champagne bottle legs, with distal wasting and preserved proximal bulk, should make you think of Charcot Marie Tooth. Finger prick marks on the fingertips or a glucose monitoring device on the upper arm raise the possibility of diabetes as an underlying cause.
Then palpate the peripheral nerves. The common peroneal nerve at the fibular head and the ulnar nerve at the elbow are the most accessible. Thickened nerves are a significant finding that narrows your differential. Charcot Marie Tooth, CIDP, leprosy and amyloidosis can all cause nerve hypertrophy.
Examine With Purpose
When you begin the formal examination, keep your five questions actively in mind. Distal weakness alone fits a typical polyneuropathy. Proximal and distal weakness together should make you think of CIDP or Guillain Barre syndrome.
On the sensory side, start distally and work proximally. Test small fibre function with pinprick and temperature, and large fibre function with joint position sense and vibration. If there is profound large fibre loss, perform Romberg's test.
Crucially, ask yourself whether the findings fit the distribution of a typical polyneuropathy or whether they fit a specific nerve or nerve root. Not all neuropathy is polyneuropathy. A dermatomal pattern of sensory loss with back or neck pain should make you think about radiculopathy. Weakness and sensory loss in a single nerve territory should make you think about an entrapment neuropathy.
The Pattern Breakers
Pattern recognition in neuropathy is not just about identifying the common presentations. It is about knowing when the pattern does not fit and being prepared to reclassify.
When it is asymmetrical, stop and reconsider. Asymmetry should make you think about mononeuritis multiplex, where individual nerves are picked off in a stepwise fashion. The causes include vasculitis, diabetes, sarcoidosis and rheumatoid arthritis. Also consider entrapment neuropathy and radiculopathy, both of which produce asymmetrical findings.
When it is purely motor, the absence of sensory involvement is your key clue. Multifocal motor neuropathy produces asymmetric purely motor weakness, typically affecting the upper limbs and is treatable with IVIg. Motor neurone disease must also be considered and here the presence of upper motor neurone signs alongside the lower motor neurone findings is the critical distinguishing feature.
When it is purely sensory, think about sensory ganglionopathy in the context of a paraneoplastic process or Sjogren's syndrome. Profound large fibre loss with sensory ataxia, a positive Romberg's test and pseudoathetosis of the outstretched hands is a striking and recognisable picture. Small fibre neuropathy is a different entity: burning pain and autonomic features with a potentially normal clinical examination.
When you find mixed upper and lower motor neurone signs, this is the most important pattern breaker of all. Brisk reflexes alongside wasting and fasciculations is not peripheral neuropathy. Your differentials must include motor neurone disease and ALS, cervical myelopathy with upper motor neurone signs in the legs and lower motor neurone signs at the level of the lesion, subacute combined degeneration of the cord from B12 deficiency affecting the posterior columns and corticospinal tracts, and syringomyelia with its characteristic cape distribution of dissociated sensory loss.
When the hereditary features are present, pes cavus and clawed toes, inverted champagne bottle legs and palpably thickened nerves should point you firmly towards Charcot Marie Tooth disease. If you are suspecting CMT, offer to ask about family history as part of your plan.
Closing the Station
When it comes to presenting your findings, use the 5 questions to put together the syndrome. “I examined [patient name], a [age and demographics] patient with leg weakness. On examination I noted they had a high stepping gait and identified symmetrical bilateral weakness in the lower limbs, which was grade 4 in the proximal muscles and grade 3 distally. There was evidence of muscle wasting and reduced reflexes in the knees and ankles. They had reduced sensation to pin prick and vibration sense to the knees bilaterally. Of note there were no upper motor neurone features, cerebellar or extra-pyramidal features. I noted that they had foot and ankle orthoses. There was also a glucose monitoring device on their upper arm. Putting this together I believe this patient has a polyneuropathy. Potential underlying causes for this include diabetes - which is my top differential here, alcohol use, or an inflammatory cause such as CIDP. To investigate this further I would take a full history from the patient, focusing on the onset, tempo and progression of their symptoms. I would also like to examine the cranial nerves and upper limbs. I would ask for a lying and standing blood pressure to assess for any autonomic involvement. I would then do blood tests including FBC, renal profile, liver profile, B12, folate, HbA1c and thyroid function tests. I perform a urine dip to look for glycosuria. I would request nerve conduction studies to see if this is an axonal or demyelinating process and would refer the patient for a therapies assessment.”
That is what a systematic, pattern based approach to neuropathy looks like. Features first, syndrome second, aetiology third.
Take It Further
If you want a framework like this for the common neurology stations in MRCP PACES, my PACES Unlocked guide covers the key examination stations with pattern recognition frameworks so you walk in knowing exactly what you are looking for.
Get your copy at medxstart.co.uk.
Frequently Asked Questions
How do you approach the peripheral neuropathy station in MRCP PACES? Start with five key questions before you examine: are the signs UMN, LMN or both? Is the pattern symmetrical or asymmetrical? Is weakness distal, proximal or both? Is there sensory involvement and what type? Are there any additional cerebellar or pyramidal features? These questions give you a neurological syndrome before you reach for a diagnosis. Look at the bedside for clues such as AFOs, pes cavus and nerve thickening before you begin the formal examination.
What causes thickened peripheral nerves on examination? Palpably thickened peripheral nerves are an important clinical finding that narrows the differential significantly. Causes include Charcot Marie Tooth disease, chronic inflammatory demyelinating polyneuropathy, leprosy, amyloidosis and neurofibromatosis. The common peroneal nerve at the fibular head and the ulnar nerve at the elbow are the most accessible sites to palpate.
What is the difference between mononeuritis multiplex and polyneuropathy? Polyneuropathy produces symmetrical length dependent sensory and motor findings, typically worst distally. Mononeuritis multiplex involves individual peripheral nerves being affected in a stepwise, asymmetric pattern. The causes of mononeuritis multiplex include vasculitis, diabetes, sarcoidosis and rheumatoid arthritis. Asymmetry on examination should always prompt you to consider mononeuritis multiplex rather than a straightforward polyneuropathy.
What does mixed UMN and LMN signs mean in the context of neuropathy? Finding upper and lower motor neurone signs together is a critical pattern breaker. It is not consistent with a peripheral neuropathy alone. The differential includes motor neurone disease, cervical myelopathy, subacute combined degeneration of the cord from B12 deficiency, and syringomyelia. Each has distinguishing features: MND has no sensory loss, cervical myelopathy produces UMN signs in the legs and LMN signs at the level of the lesion, B12 deficiency affects the posterior columns and corticospinal tracts, and syringomyelia produces a cape distribution of dissociated sensory loss.
What should you say at the end of a PACES neurology station? Always offer a structured completion. State that you would assess gait, check lying and standing blood pressure to assess for autonomic involvement, and dipstick the urine for glucose.
What is Charcot Marie Tooth disease and how do you recognise it in PACES? Charcot Marie Tooth is the most common inherited peripheral neuropathy. It causes a slowly progressive length dependent motor and sensory neuropathy with characteristic clinical features: pes cavus, clawed toes, inverted champagne bottle legs from distal wasting with proximal sparing, and palpably thickened peripheral nerves. Family history is often positive. There is no disease modifying treatment currently available.
Dr Will Bierrum is a neurology registrar and founder of MedXStart — the success platform for modern doctors, covering medical education, exams, interviews, technology, and ventures beyond medicine. medxstart.co.uk
This post is for educational purposes only. It does not constitute clinical guidelines or medical advice. Always refer to local guidelines and senior colleagues when making clinical decisions.