BMJ 2010: 341: 1111 – 1170 (27th November)

The most interesting article this week was on causes and investigation of peripheral neuropathy. My usual approach for patients with peripheral neuropathy is to send them off for random glucose, B12, and folate, and if all those are normal to leave it at that. This, it appears, is not nearly enough. Causes of bilateral symmetrical peripheral neuropathy also include:

Paraproteinaemia (9 – 10% of cases)
Alcohol abuse (7% of cases)
Renal failure (4% of cases)
HIV (16% of cases but depends on population studied)
Hypothyroidism (percentage not given, as too low to make it onto the ‘most common causes’ table, but nonetheless a possible cause)

For comparison, diabetes accounts for between 11 and 41% of cases, and B12 deficiency for a mere 3.6% of cases. So not only are all those other causes part of the differential diagnosis, but the first three and possibly the fourth are all, in fact, more likely diagnoses than one of the things I always test for.

Nor is that all. Impaired glucose tolerance and/or hypertriglyceridaemia also have possible associations with neuropathy. There’s paraneoplastic neuropathy, too. It can also be secondary to a ragbag list of diseases – sarcoidosis, Sjogren’s, and vasculitides (though those are more likely to cause mononeuropathy). And, oh, yes – let’s not forget medications (a long list of fairly unusual/obscure ones, but note metronidazole, nitrofurantoin, and pyridoxine on that list).

So, in fact, what I should be doing for my patients with numb feet is:

a) checking their medication lists and looking up the small print on side effects for each one, including an inquiry about OTC vitamin supplements;

b) making tactful inquiries into their alcohol consumption, sexual encounters, and history of IV drug use;

c) examining for sensory loss, motor loss, reflexes, and signs of cauda equina;


d) checking fasting bloods for, yes indeed, glucose and B12/folate, but also U&Es, FBC, LFTs, gamma-GT, TFTs, serum immunoglobulins, PV (er, that would be plasma viscosity, in case you were wondering), and fasting lipids, and considering HIV testing in the presence of any risk factors/other symptoms.

And, if that lot doesn’t turn up anything, I should refer – especially if symptoms are severe, rapidly progressive, or associated with motor symptoms. And consider chest X-ray for an occult cancer, methylmalonic acid to pick up that weird problem where patients have B12 deficiency despite normal B12 levels (check if B12 levels low normal), and antineuronal antibodies. It’s debatable whether nerve biopsy helps in such cases, but fortunately for me that particular decision isn’t my problem. If everything shows up negative, the default diagnosis is then chronic idiopathic axonal polyneuropathy, which from the look of it is the IBS of neurones.

Oh, yes – and Duloxetine was mentioned on the list of things to try as treatment (along with our old friends Amitriptyline, Tramadol, and Pregabalin). I did wonder whether it was worth trying it in cases of non-diabetic neuropathy.

(Edited to add: One for the reval points – had a patient in on Friday about his foot numbness and blood test results, so now I’ve been able to send him for a stack of extra investigations.)

What’s of interest in the research studies this week?

Does treatment of moderate sleep apnoea help improve hypertension? Yes, but probably not enough to count – a mere 1 – 2 mmHg on average.

If an over-80-year-old patient who’s just developed signs of a CVA questions my advice to be urgently admitted by telling me that he’s too old and it isn’t worth it, I can now assure him that research shows acute stroke treatment to work just as well in over-80s as under-80s.

Although we advise our out-of-work patients that getting back into work is better for their long-term health, it seems that the same isn’t true of patients who are out of work due to retirement rather than sick leave. Retirement apparently improves fatigue (both mental and physical) and depressive symptoms quite substantially. In France, at least.

People who believe that their substantial alcohol consumption can’t be a health problem because they only indulge in it once weekly may be kidding themselves. If your average weekly intake is high, knocking the whole lot back in your one night out and abstaining for the other six days of the week is actually worse for your heart attack risk than spreading it evenly throughout the week. Interestingly, angina risk wasn’t affected, so I suppose that must mean the effect is via a prothrombotic effect rather than an atherogenic effect. Wine drinking is still thought to be protective, though I wouldn’t aim for too much of a good thing.

Case history from Minerva: When prescribing Oilatum as a bath additive, do bear in mind that ‘bath additive’ should be taken fairly literally. If you bathe your child in a sink instead, using the amount recommended as a bath additive can lead to an excessively concentrated solution that can cause severe irritant dermatitis.

Finally, of no relevance to my CPD, but I was interested to see a comeback to something I’d been told twenty years ago. When I was at medical school, one of the pathologists told us that we shouldn’t use the term ‘autopsy’ as it would literally mean examining oneself, hard to do when you’re already dead. The correct terms, he told us, were ‘necropsy’ or ‘post-mortem’. This made such an impression on me, pedant that I am, that I’ve avoided the word ‘autopsy’ ever since. Apparently, however, what the word actually means is ‘to see for oneself’ – the ‘self’ being not the dissectee but the dissector. So there you go – now I know.


About Dr Sarah

I'm a GP with a husband and two young children.
This entry was posted in BMJ, BMJ 2010, BMJ 341, Impact, Neurology, Neuropathy. Bookmark the permalink.

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