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IntroductionWe describe two cases of valproate-induced parkinsonism, where the parkinsonian features develop after commencing valproate (VPA), in a time frame and manner well described by previous publications.1 In contrast to the published literature, that has short duration of follow-up, we have had a prolonged follow-up of these two cases, who initially improved on ceasing valproate, but then after a period progressed again, with the development of levodopa-responsive asymmetrical Parkinson’s disease.2Cases67 years old man, on VPA 500 mg twice a day for seizures since 2008, developed new rest, re-emergent left hand tremor and hypomimia in 2012. Within months, the parkinsonism progressed to decremental bradykinesia, cog-wheel rigidity and hypophonia. The symptoms initially improved with changing VPA to levetiracetam; however, the disease reappeared after 6 months and although levodopa-responsive, it has been progressive since then.88 years old man, on VPA 700 mg twice a day for seizures since 2010, developed upper limb decremental bradykinesia, cog-wheel rigidity, camptocormia and rest, re-emergent tremor in hands in 2011. The parkinsonism improved significantly with cessation of VPA; however, the disease re-emerged after 2 years and has been progressive since then.ConclusionVPA may be responsible for unmasking underlying subclinical parkinsonism and these patients represent an earlier onset of Parkinson’s disease related to VPA exposure, rather than a purely drug related parkinsonian dysfunction. These cases also highlight the importance of long-term follow up in VPA-induced parkinsonism. These observations are an important consideration for clinicians treating patients with parkinsonian features secondary to VPA exposure.ReferencesBrugger F, Bhatia KP, Besag FM. Valproate-associated parkinsonism: a critical review of the literature. CNS Drugs 2016;30(6):527–540.Mahmoud F, Tampi RR. Valproic acid-induced parkinsonism in the elderly: a comprehensive review of the literature. Am J Geriatr Pharmacother 2011;9(6):405–412.

Background: Multiple sclerosis (MS) is an autoimmune inflammatory demyelinating disease that causes significant disabilities. Latest MS epidemiological data in Australia reveal rising prevalence. No epidemiological study of MS has been conducted so far in the Illawarra region.Aim: To calculate prevalence and incidence of MS in the Illawarra region and compare with data from other regions, states and the national prevalence.Methods: Data of MS patients in the Illawarra region were collected from hospital medical records, ambulatory care units and hospital pharmacy. Prevalence was calculated for alive MS patients on 30 June 2018 expressed per 100 000 population. Yearly adjusted incidence rate was calculated for 10 years (2009)(2010)(2011)(2012)(2013)(2014)(2015)(2016)(2017)(2018)(2019), expressed as cases per 100 000 population-years.Results: Estimated MS prevalence in the Illawarra region was 116.6 per 100 000 population with yearly incidence (2009-2019) of 5.06 cases per 100 000 population-years (female to male, 3:1). Relapsing-remitting MS (RRMS) was the most common type (277/ 397; 69.7%) with primary progressive MS (PPMS) in 52/397 (13%), and secondary progressive MS (SPMS) in 45/397 (11.3%; unknown in 23). The commonest age at diagnosis ranged between 30 and 39 years for all types with RRMS and PPMS between 30-39 years and 40-49 years respectively. The most common recorded treatment was natalizumab (103 patients), followed by fingolimod (82 patients) and interferon (58 patients). Conclusion:The calculated MS prevalence in the Illawarra region is higher than New South Wales and the Australian average MS prevalence. Further epidemiological studies focussing on MS risk factors and other factors bearing on MS prevalence in the Illawarra region are required.

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disorders of connective tissues. Nasal CSF leakage is extremely rare. 1 Methods and results We present the case of a 40-year-old woman presented to hospital for few days history of postural headache associated with clear intermittent discharge from right nostril without any signs of meningism. There was no history of trauma. She has a background history of Marfan syndrome with associated complications of ASD repair at age 2, mechanical Aortic and Mitral valve replacement, aortic root repair, previous ST elevation MI with LV dysfunction, automated implantable cardioverter-defibrillator in situ, atrial fibrillation, and Hashimoto's thyroiditis. Her regular medications are warfarin, bisoprolol and thyroxine. The clear nasal discharge was positive for b-2 transferrin confirming cerebrospinal fluid. Her CT Brain did not reveal any clear site of CSF leak. She had a flexible nasendoscopy which showed normal nasal passageway, no defect in nasal mucosa and no active CSF leakage. She was managed conservatively with strict bed rest and advised to minimise strenuous activity and heavy lifting. Conclusion Spontaneous cerebrospinal fluid leak is uncommon condition and frequently associated with hereditary disorders of connective tissues. Nasal CSF leakage is extremely rare. 1 Testing b-2 transferrin has high sensitivity and specificity. 2 Initial treatment may include bed rest, oral or intravenous hydration, oral caffeine or corticosteroids. 3 4 If conservative therapy fails, surgical repair with nasal endoscopic approach is recommended. 2 5 REFERENCES 1. Ommaya A, Di Chiro G, Baldwin M, Pennybacker J. Non-traumatic cerebrospinal fluid rhinorrhoea.