RESUMO
BACKGROUND: Functional neurological symptom disorder (FND) is characterised by neurological symptoms that are incompatible with recognised neurological or medical conditions. The condition is common in neurology clinics and causes significant morbidity, though timely access to specialist care is difficult. We sought to characterise the availability and clinical practice of specialist FND clinics across Australia and New Zealand. METHODS: Clinicians or coordinators involved in running specialist FND clinics were identified through clinical contacts with further recruitment by snowball sampling and contacting patient organisations. All clinics completed a survey about details of service delivery, including clinical model, referral sources, criteria, demand, staffing, interventions, clinical data collection, and funding. RESULTS: We identified 16 clinics across Australia and New Zealand. Of these, 12 were in capital cities and four were in regional centres. Three of these focused on paediatric patients and 13 focused on adults. Clinics varied in their clinical model, referral sources, criteria, staffing, interventions, data collection, and funding. Most clinics reported challenges related to coping with demand and obtaining adequate funding. CONCLUSION: FND clinics in Australia and New Zealand appear to be concentrated predominantly in metropolitan areas and vary considerably in their referral sources, clinical data collection, and models of care. Reported challenges in meeting demand indicate a need for greater resources. The heterogeneity across clinics suggests a need to harmonise clinical standards to facilitate access to evidence-based care.
RESUMO
Intracellular aggregates of α-synuclein are the pathological hallmark of Parkinson's disease (PD) and dementia with Lewy bodies (DLB), being linked to neurotoxicity. Multiple triggers of α-synuclein aggregation have been implicated, including raised copper. The potential protective role of the endogenous copper-/zinc-binding proteins, metallothioneins (MT), has been explored in relation to copper-induced α-synuclein aggregation. Up-regulated endogenous expression of MT was induced in SHSY-5Y cells by the synthetic glucocorticoid analogue, dexamethasone. After treatment to induce endogenous MT expression, immunofluorescence confocal microscopy was used to quantify protein aggregates in cells with/without copper treatment. MT induction resulted in significant (p < 0.01), dose-dependent up-regulation of MT expression and significant reduction in Cu-dependent α-synuclein intracellular aggregates (p < 0.01) that could be suppressed by MT-specific siRNA. Ubiquitous (MT-2) and brain-specific (MT-3) isoforms were investigated by transient transfection of the GFP-fusion proteins, observing equivalent α-synuclein aggregate suppression by each. These studies indicate MT induction could have potential in PD/DLB neuroprotective therapy by suppressing α-synuclein aggregation.
