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Nomination for ABN Honorary Secretary and Honorary Treasurer are now open. Please do consider if you could stand, or could encourage a colleague to stand for these important roles.

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Events

Save the date Wednesday 9 - Friday 11 May 2018.

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2016 Winners

Winners of the Undergraduate Prize 2016:

Clinical Case: Amine Awad

Research:  AK Hari Narayanan

Audit:  Kevin Teo

 

Amine Awad

Clinical Case

Two Cases of Mild Encephalopathy with Reversible Splenial lesion (MERS) in two UK Teaching Hospitals

Summary

Mild Encephalopathy with Reversible Splenial lesion (MERS) is a clinical-radiological syndrome characterized by an acute encephalopathy with radiological evidence of a reversible lesion in the splenium of the corpus callosum (SCC). Since first described in 2004, MERS has almost universally been reported in East Asia. We report two cases of para/post-infectious MERS in the UK.  Case 1, a 13 year old African-Caribbean boy and Case 2, an 11 year old Caucasian girl with ulcerative colitis controlled with mesalazine and mercaptopurine, presented with encephalopathy, ataxia, and pseudobulbar features. Case 1 was febrile. Case 2 had an afebrile prodrome with sore throat, vomiting and diarrhoea. Both received treatment with acyclovir and cefotaxime. The only abnormality on lumbar puncture was 10 white cells in the cerebrospinal fluid of case 1, and viral PCRs were negative. In both children, MRI revealed abnormal signal on T2/FLAIR and diffusion-weighted imaging in the SCC with no gadolinium enhancement, with Case 2 showing additional abnormal signal in the cerebellar hemispheres. Both received a course of intravenous methylprednisolone, 1g OD, for 3 and 5 days respectively. Case 1 had evidence of a recent Mycoplasma pneumoniae infection (serum IgM antibody titre 1/640), and made a full recovery by the end of a 2 week admission. Case 2 had residual upper limb dyspraxia and mild cognitive problems 5 weeks after onset of symptoms. The two cases add to the number of cases of MERS reported outside of East Asiaand highlight MERS as a differential for para or post-infectious encephalopathy.

  

AK Hari Narayanan

Research

Investigating the Pathogenesis of Vascular Parkinsonism (VaP): Does Neuroinflammation Matter?

Summary

Vascular Parkinsonism (VaP) is a progressive neuromotor disorder affecting the elderly. VaP is associated with small vessel disease (SVD) in the basal ganglia but the exact mechanism of nigrostriatal impairment is unknown. A pre-clinical model of hypoperfusion suggested hypoxic damage in the dorsal striatum could cause nigrostriatal degeneration. The evidence of IL-1β mediated neuroinflammation in this model suggested that microglial activation can contribute to the pathogenesis of parkinsonian syndromes. No studies have investigated in detail the neuropathological substrate of VaP in human tissue. Eleven cases of VaP and four cases each of age-matched controls, early (Braak III) and late (Braak VI) stage idiopathic Parkinson’s Disease (iPD) were selected out of 819 brains from the Parkinson’s UK Tissue Bank at Imperial College, London. Large sections from the medial and posterior basal ganglia were studied with immunohistochemistry using markers for microglia, reactive astrocytes and the inflammasome protein ASC that signifies IL-1β activation. Synaptic and dopaminergic terminal density were also investigated. Immunostaining was quantified via ImageJ. A two-fold increase in microglia was seen in VaP compared to early and late stage PD, while astrocytosis was uniform. ASC was expressed in microglia suggesting the production of IL- 1β. A 10-fold loss of dopaminergic neurones were observed in the putamen and internal pallidus in VaP compared to PD, while a uniform loss of synaptic density was observed in all disease states. Dopaminergic terminal loss in VaP, similar to PD, indicates that chronic hypoperfusion, secondary to SVD, and neuroinflammation is the cause of VaP.

 

Kevin Teo

Audit

Management of thin saliva symptoms in patients with Motor Neurone Disease

Summary

Excess thin saliva symptoms cause significant morbidity in patients with Motor Neuron Disease (MND) and there is no good consensus with regards to medical management of such symptoms. This cross-sectional study aimed to assess the prevalence and time to onset of saliva symptoms in MND patients with various presenting symptoms.  It also evaluated the prescribing practices for thin saliva symptoms in Addenbrooke's MND Care Centre and those of neurologists in East Anglia with reference to the current 2016 NICE guidelines.
44.2% of MND patients (n = 86) were found to experience saliva symptoms during their disease course. Bulbar-onset MND patients were found to have a significantly shorter time between the onset of the first symptom to the development of salivary symptoms as compared to spinal-onset MND patients (14 ± 2.3 months versus 39.5 ±9.8 months).  It was found that the first- and second-line treatment of choice for thin saliva symptoms of neurologists in East Anglia involved trialing various preparations of anticholinergic agents.  Of the anticholinergic preparations used, atropine eye drops and amitriptyline were best tolerated judging from discontinuations and numbers reporting side effects.  Four out of six neurologists would only consider using or referring patients for intraglandular botulinum toxin (BoNT) injections following failure of anticholinergic therapy. Concern over possible side effects and lack of adequate staff training accounts for the discrepancy between NICE recommendations and current utilisation of BoNT therapy for thin saliva symptoms. 

 

News

Nomination for ABN Honorary Secretary and Honorary Treasurer are now open. Please do consider if you could stand, or could encourage a colleague to stand for these important roles.

Read More

Events

Save the date Wednesday 9 - Friday 11 May 2018.

Read More