17 Aug, 11 | by Professor Matthew Kiernan, Editor of JNNP
This week we have a post from Dr Arun Krishnan, Web Editor at JNNP:
Over the last few weeks, I have been helping train and examine candidates for the specialist entry exams for the Royal Australasian College of Physicians. The candidates are fully qualified doctors with 3-4 years of hospital experience, who are planning on entering speciality training in an internal medicine discipline. All have extensive training in general medicine and a few, no doubt, will have spent time in Neurology rotations along the way. None of these doctors are neurologists and only a handful of successful candidates will choose to apply for Neurology training in the future.
Despite this, the enthusiasm for detecting neurological signs has been at an all time high. There has been much consternation about signs: is the weakness truly pyramidal, is there 3mm or 4mm of proptosis, does the patient with the third nerve palsy have sparing of the 4th nerve and finally of course, la pièce de résistance – are the plantars truly extensor 1? I have been unsure how to deal with this sudden reliance on physical signs: should I step in and tell them that it is wonderful to see such unbridled enthusiasm and that Sir William Gowers would have been proud or should I break it to them that none of this really matters in 2011 once you have had an MRI of every neuron and axon, a full genetic ‘panel’ including testing for conditions that have only ever been described in a single North African family and biopsies of muscle, nerve and skin (don’t forget CADASIL2 as a potential cause of migraine…in anyone… ever..).
While these thoughts are not without a degree of elaboration, the fact remains that there is little uniformity, even amongst clinicians at the same institution, as to what constitutes an adequate neurological examination. This issue was raised in a general medicine meeting at an institution where I trained some years ago. On that day, a non-neurologist said that his documentation of a normal neurological examination was summarised in two words: ‘CNS- NAD (no abnormal detected)’. Another argued that this was completely misguided and that a more accurate description should be given such as ‘CNS ü’. Of course, it will be argued that the examination needs to be tailored to the problem, but that is exactly where the debate starts. Just how much do you examine in a patient with migraine or epilepsy, where not infrequently, the ‘general’ neurological examination is normal? Moreover, are we spending too much time focussing on signs in an era where counselling patients, discussing test results and monitoring for medication side effects are becoming increasingly time-consuming?
Clearly there are also cultural factors that weigh heavily on this. As a medical student, I spent time on an elective rotation in Chennai, India. Patients were not at all fussed about being seen in 5 minutes and discharged from clinics, as long as the neurologist examined them. Failure to examine was associated with pleas from patients, who clearly felt that ‘healing hands’ were all they needed. Also, the current focus on extensive investigation seems untenable, especially in the developed world where an ageing population will place huge pressure on resources. Surely, there is a need to stratify investigations on the basis of clinical signs.
Moreover, in many countries, especially in the developing world, I would suspect that the growing Western philosophy of “investigate first, examine second” is completely impractical. How extensively do clinicians examine in these settings? Are we simply better doctors for examining more, rather than less? Or is this merely a question of timing? In future generations, perhaps we will tell budding doctors something along the following lines: “show me the MRI and I will tell you which direction those plantar responses are heading.”
1. Lance JW. The Babinski sign. J Neurol Neurosurg Psychiatry. 2002 Oct;73(4):360-2.
2. Tournier-Lasserve E, Joutel A, Melki J, et al. (March 1993). “Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy maps to chromosome 19q12”. Nat. Genet. 3 (3): 256–9.