Association of British Neurologists Trainee Afternoon

Posted in Courses & Conferences on 19th Sep 2015

Conference details: 19 May 2015, Harrogate, UK.
Report by: Chinar Osman, Neurology SPR, Southampton General Hospital.

ACNR-SO15-full-high-rez-27I attended the Association of British Neurologists trainee afternoon on Tuesday 19th May 2015 in Harrogate. I must say I found it to be very useful and relevant to clinical practice. It was a mixture of cases with interactive small group discussions.

The first part entailed small group teaching sessions on muscle diseases. We were divided into four groups depending on our level of training. The sessions were delivered by Professor Doug Turnbull from Newcastle, Dr Paul Maddison from Nottingham, Dr Mark Busby from Leeds and Dr John Walters from Swansea. They were rotating between groups and presenting cases for discussion. The first case was a patient with a diagnosis of chronic progressive external opthalmoplegia. They explained the different genetics in this condition, which can have an effect on prognosis. For instance, if the patients have a large single deletion in mitochondrial DNA, this can increase the chance of serious cardiac conduction abnormalities and the 3243 mutation carries a poorer prognosis. The second case was rhabdomyolysis in a 27-year-old patient with learning difficulties and scapula winging who was found to have a limb girdle muscular dystrophy. We discussed the importance of history taking in muscle patients and also the need to establish if there are any clues in the history regarding the ‘second wind’ phenomenon, which can affect patients with McArdle’s disease. The third case was a patient who was found to have a laminopathy where the nuclear laminar and associated proteins such as emerin are affected. Once again, this case highlighted the importance of genetic testing for various genetic subtypes, which can cause significant cardiac abnormalities such as LGMD1B. The fourth case was a patient with chronic fatigue and aches with mild calf hypertrophy and a persistently raised CK. A muscle biopsy with immunohistochemistry showed dystrophin, highlighting the importance of performing immunohistochemistry to look for muscle integrity.

The second session was a lecture by Dr Gillian Sare from Nottingham on ‘Moving Towards Consultancy’. This was a well-delivered and relevant talk. It outlined important interview skills as well as being an eye opener of what one needs to do to prepare for consultancy.

Following a well-deserved coffee break, the third session was again small group teaching sessions on dizziness in the general neurology clinic. The sessions were delivered by Dr Geraint Fuller from Gloucester, Dr Nicola Giffin from Bath, Dr Ralph Gregory from Poole and Dr Mark Lewis from Leeds. They were rotating between groups and presenting cases for discussion. The first case was a patient with acute vertigo with BPPV who had a positive Hallpike. We were shown how to do the Dix Hallpike and the therapeutic Epley manoeuvre. The second case was a Parkinson’s patient complaining of dizziness. We discussed different mechanisms of dizziness in Parkinson’s disease, varying from polypharmacy to postural hypotension and postural instability. The third case discussion was on how to differentiate between peripheral and central causes of vertigo. If the patient had a negative head thrust test with direction change nystagmus and a skew deviation then it is likely to be a central cause. The fourth case was a case of vestibular migraine with a combination of vertigo, balance disturbance with migraines. It is still under-diagnosed and the management is similar to migraines. There is also no strong evidence of risk of stroke if you are a migraine sufferer unless you are female and on the combined oral contraceptive pill.

During the second part of the afternoon we were joined by the foundation/core medical trainees and had a lecture by Prof Doug Turnbull and Dr Paul Maddison on red flags in muscle disease and top tips for neurology examination. This was primarily aimed at muscle diseases and I felt was slightly high powered for the foundation trainees. 1 in 4000 have a mitochondrial disease and the commonest mitochondrial disease is Leber’s Hereditary Optic Atrophy and 3243 mutations. Patients with MELAS (Metabolic encephalopathy lactic acidosis and stroke like episodes) have 3242A mutation in 80% and they need optimum seizure control. If patients have a POLG mutation and have seizures one must avoid sodium valproate. Patients with 3243A mutations can have gastrointestinal muscle involvement, thus impeding peristalsis, so it is important to prevent constipation. We were also taught about the importance of distribution of weakness to help establish a diagnosis. For instance, in inclusion body myositis, the distribution of weakness is variable and can be asymmetric, with early weakness of knee extensors and ankle dorsiflexion and the weakness of wrist and finger flexors is disproportionate to the extensors. Therefore, they complain of dexterity loss and grip strength. Finally, they discussed the significance of CK in certain conditions and the importance of always checking thyroid function tests in a suspected high CK as hypothyroidism can raise CK.

Following some light refreshments, Professor Alastair Compston delivered a lecture on ‘Translational Neurology in Action – Campath-1H’. The history of which backdates to 1984 (The year I was born!) where its original intention was to treat leukaemia. This was the first human monoclonal antibody (CD52) used as a treatment for multiple sclerosis (MS), with the first MS cohort treated in 1991 and it was soon found to be beneficial in early relapsing remitting MS (RRMS). However thyroid autoimmunity is a common (30%) complication after two years of treatment. In 1999 patients were being treated very early in the disease and it showed a good response with expanded disability status scale (EDSS) improvement. Later named Alemtuzumab this was trialled in RRMS in phase II trials, which showed superiority over Rebif (interferon beta-1a). Alemtuzumab improved natural history for up to 15 years post therapy. The current aim is to help identify patients in advance who could be at risk of autoimmunity following treatment.

We then had a talk on ‘Running a Multicentre Study’ by Professor David Burn from Newcastle who explained all the important components of running a study and was an insight into real research.

The last talk was ‘Lessons I’ve learned from my PhD and beyond’ by Dr Jon Rohrer from London. This was a great way to end the evening as it helped guide us on how to approach research and the important factors to consider.

So all in all this was certainly a packed and useful trainee session which was a good kickstart to the meeting ahead!

ACNR 2015;15(4):27.  Online 19/09/2015

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