I know – it is supposed to be a Saturday night palsy, but as you know patients rarely bother to read the textbook before injuring themselves or falling victim to circumstance.
I was working on a Monday recently, which is weird as I try to avoid Mondays. A 23 year old woman presented to ED with a profound wrist drop and some paraesthesia to the dorsal hand. She was otherwise fit and healthy and had the classic history of having a few too many ales on the night before – which resulted in her falling asleep in an uncomfortable position of the side of a fold-away sofa bed.
When she woke she felt a dull ache in her upper arm and could not extend her wrist. She shook it off and tried to do some exercises but 2 hours later it remained quite flaccid to extension and was becoming a bit worrying.
Now if you are not familiar with this syndrome – this is classical “Saturday Night Palsy” of the radial nerve. Or is it?
I was always taught that this neurological phenomenon occurs when one overindulges in alcohol and falls asleep with the arm draped over the edge of a chair / bench / fence… causing a compression of the radial nerve as it traverses the spiral groove around the humerus. It is also known as “honeymoon palsy” where newlyweds sleep together in an awkward embrace and one get their nerve squashed in an effort to remain romantically entwined with their new love. I have also seen the term “Crutch palsy” where folks misuse crutches for leg injuries and place the top buttress of the crutch up into the axilla [not on the chest wall] and squash the posterior cord of the plexus. We also see traumatic radial nerve injury after fractures of the mid shaft of the humerus – but these are easier to diagnose the cause!
However, the story is as usual – more complicated. This diagnosis has a rich and long history going all the way back to the ancient Greeks.
Turns out it may have originally been titled “Saturnine paralysis”. Saturn is the seventh planet and lead was the “7th metal” in ancient times. So men who drank beer that had settled in pewter mugs were prone to lead poisoning – they were described as being “saturnine” – like the dark and ghoulish Roman God. The whole Roman Empire may have been in part decayed by the lead in the plumbing [plumbum is Latin for lead, and the root of the English word – plumbing] This continued through the Middle ages with “adulterated wine” being the source of mass poisonings throughout Europe. Facial whitening preparations were common sources of lead toxicity in Europe and Asia – Elizabeth the First a notable user / ? sufferer. In modern times we were still exposing ourselves to lead in paint and fuel additives up until very recently. In parts of Western Africa the “underground” mining of lead still causes significant burden in the children of the villages.
Lead toxicity, in adults, tends to cause a peripheral neuropathy involving the extensors of the wrist and fingers in the first instance before spreading to other areas. (kids tend to get central CNS toxicity though – see Dr Natalie Thurtle’s SMACC talk on that.)
So how did the term “Saturday Night palsy” enter the English language? Well, if you believe the etymologists there may have been a confusion between the French ‘paralysis saturnine’ and ‘Saturday palsy’ which over time as the incidence of lead toxicity decreased became synonymous with the modern “Saturday night phenomenon” which still involves the drinking of excessive alcohol, but causes the wrist drop in a more acute and unilateral fashion. [If you want to read more check out this fascinating article by Spinner et al in NeuroSurgery 2002]
OK, back to the case. We have a story that sounds like the perfect set up for “Saturday Night palsy” – alcohol to excess, sleeping in an awkward position with pressure on the posterior upper arm. Her neurological examination showed preserved elbow extension, some weakened supination and flaccid weakness of the wrist and finger extensors. This is typical for a lesion in the spiral groove below the supply to the tricep muscles. [Han et al have a great review article in Journ Korean Neurosurg, 2014 here]
Importantly our patient did not have any symptoms and had a normal examination of the other arm…. would be bad to miss the lead tox! OR possibly some other symmetrical demyelinating process? One should always keep diabetes, thyroid disease and B12 in the back of your mind when seeing symmetrical peripheral neuropathies.
So it was a slam dunk diagnosis – clinical medicine, applied anatomy and history all coming to gather to allow me to say – this is a radial nerve palsy…. but before I indulge in too much self-congratulation… I had to admit that I had absolutely no idea what to tell the patient about what I could do for her or how this was going to to turn out in the future.
So off to the books to learn the facts so I could inform the patient. Turns out that the data is actually pretty limited – just a few case series and reviews, mostly with a strong neurological theme of looking at action-potential conduction recovery rather than patient recovery!
The news is good – the vast majority of patients with “non-traumatic” radial nerve lesions make a full recovery. As one would expect it does take time for the nerves to regenerate – and the studies I read ranged from 2 weeks out to 6 months for a full recovery of function. The mean duration of symptoms was around 3 months in most reports. So what can we do in the meantime?
The mainstay of treatment involves:
Splinting to maintain the tendons, joints and allow some function as the wrist drop resolves. Our best friends here at the OTs or hand therapists. They can make customised, dynamic hand splints that keep the joints moving and allow exercises which maintain the tendons etc.
Passive exercises to keep the muscles moving and avoid atrophy where possible to enhance recovery as the nerve supply comes back online.
So when I discussed this case with the “local” Neurologist (2000 km away) they were keen to get an MRI and nerve conduction studies. This seems like a good idea, mainly to exclude other nasty or unexpected causes of nerve compression. However, I do wonder, in a disease with such a good prognosis and relative fast recovery where the diagnostic testing is unlikely to change our immediate management… is it really worth it?
Would it be best to do all the tests up front? Or should we reserve these for cases where there is not recovery as expected or the story doesn’t make sense in terms of aetiology?
I am a GP working in Broome, NW of Western Australia. I work as a hospital DMO (District Med Officer) doing Emergency, Anaesthestics, some Obstetrics and a lot of miscellaneous primary care. Also on the web as @broomedocs | + Casey Parker | Contact