Wednesday, 31 August 2016

TB & parainfectious myelitis

Why are absent sensory nerve action potentials such an important finding in cases of myelitis? #TeachNeuro

I saw a patient last week on the ward with necrotic myelitis with lower motor neurone signs in the lower limbs and mixed upper and lower motor neurone signs in the upper limb. He had a sensory level at C8/T1 and a motor level at C7/C8. The presumptive diagnosis has been TB myelitis based on low CSF glucose level compared to the peripheral blood and raised total protein. CSF cultures have been negative and a peripheral screen has not shown systemic TB, including a whole body FDG-PET study. When I trained in South Africa I saw several cases of so called TB-related parainfectious myelitis. These patients all had active TB and developed their myelitis shortly before, or after, starting their anti-tuberculous drugs (see article by Silber et al. 1990). The hypothesis underlying these cases is that the myelitis is a monophasic autoimmune disease. Mycobacteria are potent adjuvants and are well known to trigger, or boost, autoimmune responses in animals. In fact, complete Freund's adjuvant (CFA or FCA) is composed of inactivated and dried mycobacteria (usually M. tuberculosis) in an oil emulsion. CFA is often referred to as the immunologist's dirty little secret and is what is used to trigger EAE (experimental allergic encephalomyelitis).

The one red flag in relation to this patient is that his nerve conduction studies show absent SNAPs (sensory nerve action potentials) in the lower limbs and a whole body work-up has not shown peripheral TB. Why is finding absent SNAPs such an important clue in this case?

Essential Reads

Silber et al. Neuromyelitis optica (Devic's syndrome) and pulmonary tuberculosis. Neurology. 1990 Jun;40(6):934-8.

Neuromyelitis optica and acute necrotic myelopathy occur in association with pulmonary tuberculosis. We studied 8 patients with either neuromyelitis optica (6), acute myelopathy (1), or acute optic neuropathy (1) in close temporal association with pulmonary tuberculosis, but with no evidence for CNS tuberculosis. Neurologic symptoms preceded the use of antituberculosis medication in 5 patients. Different patients showed similar clinical features, suggesting a consistent disease pattern. Autopsy examination (1 patient) revealed extensive spinal cord and optic nerve demyelination. We identified only 5 additional patients seen over the same period with idiopathic neuromyelitis optica, thus suggesting that the close temporal relationship to pulmonary tuberculosis is not coincidental. The syndrome is most likely due to an immune reaction to tuberculosisrather than the use of antituberculosis medication.

Hughes & Mair. Acute necrotic myelopathy with pulmonary tuberculosis. Brain. 1977 Jun;100(2):223-38.

Tuesday, 30 August 2016

Thursday Neuroscience Clinical Meeting - Governance, Audit & Neurology Consultants’ meeting

Date: Thursdays
Time: 09:15 - 11:30 am
Venue:   Princess Alexandra House lecture theatre, Ashfield St
Details: Governance, Audit & Neurology Consultants' meeting

Getting to The Royal London Hospital 


The hospital is located very close to the Whitechapel underground station. It is served by the Hammersmith and City and District lines as well as the London Overground. 


The following buses stop outside or close to the hospital on Whitechapel Road: numbers 25, 106, 205, 253 and 254 as well as night buses N25, N106 and N253. Bus numbers 15, 115 and D3 stop close to the hospital on Commercial Road. Low-floor wheelchair accessible buses run on all routes serving The Royal London Hospital. 

Pedestrian access: 

The main hospital building can be accessed from Whitechapel Road or Stepney Way. 

The Outpatients Department building can be accessed from Stepney Way.  


There is no public parking at the hospital itself, but there is metered parking in surrounding streets.  

Clinical Skills: auscultation of the heart

Do you know how to interpret auscultation of the heart? #TeachNeuro

I have very fond memories of learning auscultation of the heart from one of the most astute cardiologists of his generation, Professor John Barlow, at the University of the Witwatersrand. Professor Barlow's clinical skills were legendary and there was nothing more entertaining than attending his cardiology rounds at Baragwanath hospital. I recall him on more than one occasion accurately predicting the pressure gradient across a tight aortic stenosis and on several occasions he even outperformed the earlier generation echo machines. I recently repurchased Professor Barlow's album on the auscultation of the heart. I sincerely hope you enjoy listening to it as much as I did as a medical student. The aim of this post is not hark back to a previous era of medicine, but to learn from the giants of our field. Although cardiac auscultation is a dying skill knowing how to auscultate and interpret the findings reinforces important aspects in relation to the neurophysiology and physiology of the heart. Enjoy.


Functional Neuroanatomy

Functional #neuroanatomy is a core skill for all neurology trainees. #TeachNeuro

I remain flabbergasted by the response I recently received from a trainee neurologist when I asked him how he would localise the anatomical site of a IIIrd nerve palsy. His response: “I would order an MRI scan to localise the lesion”. What is happening to our basic neurological skills? It has become clear to me that basic neuroanatomy knowledge amongst most neurology trainees is rudimentary, and is simply not detailed enough, to assist in the anatomical localisation of lesions.  I am therefore proposing that all trainees relearn functional neuroanatomy in a way that is designed to augment their skills in undertaking and interpreting the neurological examination. The following is a list of questions all neurology trainees should be able to answer: 
  1. What does a IIIrd palsy look like?
  2. What are the clinical features of a lesion involving the nucleus of the IIIrd nerve?
  3. How do you localise a brainstem, or fasicular, IIIrd nerve palsy?
  4. How do you localise a third palsy to the subarachnoid space?
  5. How do you assess a the function of the trochlear nerve (IVth) in the presence of a IIIrd nerve palsy?
  6. What features helps localise the IIIrd palsy to the cavernous sinus?
  7. What is the significance of a pupil sparing IIIrd palsy? 
  8. What is the significance of fixed mid-sized pupil in association with a IIIrd palsy?
  9. What are the features of a palsy of the superior division of the IIIrd nerve?
  10. What are the features of a palsy of the inferior division of the IIIrd nerve?
  11. How do you localise a IIIrd nerve palsy to the superior orbital fissure? 
  12. Is diplopia and invariable clinical feature of a IIIrd nerve palsy?
  13. Can you describe the anatomy of the the IIIrd nerve?
  14. Can you describe the paths of the parasympathetic and sympathetic innervation of the eye?
When I get the time I will produce a simple one-page infographic to answer all these questions. Does anyone want to help? I feel so strongly about this that I will be writing a commentary for Practical Neurology on this issue.