brainWAVES The Newsletter of the Brain Foundation
Winter 2015
MAJOR RESEARCH GIFT Congratulations Dr Neil Spratt, University of Newcastle
The Board of the Brain Foundation recently announced a major research gift, to the value of $300,000 over a three year period, to go to research that exhibited great potential for improved patient outcomes.
Dr Neil Spratt with Brain Foundation Secretary General, Gerald Edmunds at ANZAN.
We received many competitive applications Australia wide, posing a challenge for our Scientific Committee to make a selection. We would like to thank the North West Committee of the Brain Foundation (organisers of the annual Tamworth Fair) for their very generous contribution to this award.
Congratulations to Dr Neil Spratt who was awarded this significant grant, formally announced at the Annual Neurology Conference in Auckland during May.
Major Research Gift – Lay Summary
A new understanding of increased pressure within the skull in brain diseases
The Brain Foundation is Australia’s only research organisation that independently awards grants to all areas of brain disorder and disease.
The skull encases and protects the brain, but after injury, increasing pressure within the skull can reduce blood flow and worsen injury. As occurs elsewhere in the body, when the brain is injured (from e.g. trauma, stroke or bleeding around the brain) swelling occurs.
With the government cutting available medical research funding and with brain disease receiving less than 5% of this funding, we are now more important than ever.
Because the skull is basically a ‘closed box’ this swelling can cause a pressure rise. This has been recognised as a problem for more than a century. However, we have made recent experimental discoveries that show that pressure rises even after small stroke without noticeable brain swelling. We were suspicious that this pressure rise may be related to increases in the volume fluid around the brain – the cerebrospinal fluid. We found that there is a substance within this fluid that can trigger the pressure rise.
Dementia (including Alzheimer’s) alone, is the second leading cause of death in Australia. Dementia is not a natural part of ageing. Many diseases can cause dementia. Research is the only way we can understand the causes and identify strategies for prevention and treatments. And this is only one disease. There are hundreds more – Brain Tumours, Traumatic Injury, MND, Migraine & Headache, Stroke, Aneurysms, Parkinson’s and Dystonia to name some better known ones.
Excitingly, our experimental studies also show that the pressure rise can be completely prevented by a short duration of body cooling. Dangerous pressure rises are also an important feature of multiple other
Dr Neil Spratt at the University of Newcastle
brain diseases, and existing treatments are limited. As in stroke, causes other than brain swelling have not generally been considered. In this project we will determine the best way to apply cooling, as a precursor to clinical trials; we will explore the mechanisms causing the rise, in order to develop additional therapies; and we will determine whether this newly identified mechanism contributes to pressure rise in other brain disorders. I would like to thank the Brain Foundation for the opportunity to pursue this exciting research.
If you or a family member were to become afflicted by any one of these diseases, wouldn’t you want a successful treatment option? Help us to find them.
Contact the Brain Foundation PO Box 579, Crows Nest NSW 1585 Telephone: 02 9437 5967 or 1300 886 660 Email: info@brainfoundation.org.au Visit our websites brainfoundation.org.au and headacheaustralia.org.au
Dystonia News DYSTONIA: Muscles Behaving Badly Dystonia is the third most common movement disorder worldwide. Following is an interview with Prof. Lynley Bradnam, Professor of Physiotherapy, UTS, and recipient of Brain Foundation research grants in 2011 & 2012. For further information about Dystonia please email Lee Pagan at ADSG@live.com.au
Deconstructing Dystonia Your latest research focuses on cervical dystonia. Can you describe what this is? Cervical dystonia is a neurological condition, which causes abnormal postures of the neck, usually twisting, and sometimes with tremor. It's painful, and there are very few treatment options. It commonly comes on in your late to mid30s or early 40s and you have it for the rest of your life. People with dystonia have trouble with everyday activities, such as driving, sleeping, and crossing the road, and some people are in constant pain. They find it very difficult to be in crowded places; they have a lot of problems with their body awareness and their spatial perception. If they have to do something stressful it'll often make the dystonia symptoms a lot worse. Many people retire early because they can't maintain their job due to the dystonia and the stress that goes with it. The prevalence is low, only about 1 person per 5000 has dystonia. But for those that do, it's very distressing, and it impacts highly on their quality of life.
The upcoming Parkinson's Australia National Conference will include several dystonia presentations, including one by yourself; how has dystonia come to be associated with Parkinson's disease? Quite often when people talk about Parkinson's, they say 'and other movement disorders' and that appears to be where dystonia gets lumped.
of your studies involving this technique? I use TMS, and also transcranial direct current stimulation, and they are both methods where you can stimulate neuroplasticity in the brain, so you can put it over an area of the brain and make it either more or less excitable depending on the configurations and timings that you use.
Both dystonia and Parkinson's affect the basal ganglia. But with Parkinson's we know that there's a certain area of the basal ganglia where the neurons degenerate and so dopamine isn't produced in the brain. Parkinson's can be treated symptomatically with dopamine drugs, which can improve symptoms for some people. With dystonia, the basal ganglia are likely involved but there's never been any sign of any degeneration within the basal ganglia. It's much harder to pinpoint exactly what the pathophysiology is; something is going wrong in the same part of the brain, but it's inherently different because one's degenerative and one isn't.
About four years ago, I got a small grant from the Brain Foundation to have a look at stimulating the cerebellum in people with focal hand dystonia, and then I got a second grant in 2012 to look at the same thing in people with cervical dystonia.
You have been undertaking research on a method of brain stimulation-transcranial magnetic stimulation (TMS)-which will form part of your presentation; what have been some of the key outcomes
The subjects had 1O sessions in a row of having their cerebellum stimulated, and then we followed up with exercises and laterality training. Half of them got real brain stimulation and the other half got sham stimulation, and we saw a significant difference in the quality of life measure that we used between the real and the sham groups. It seems to have quite a marked effect on the pain that they experienced as well as their quality of life. The conference will be the first time those results are formally presented. What other areas have you been examining? I've been looking at visionrelated quality of life in people with
dystonia; how having your neck twisted all the time affects your ability to see, and then how that impacts on your ability to function; that's a study we're undertaking at the moment. The other work I'm doing is looking at gait and balance and reaction. Stepping time, because no work has done on how neck dystonia affects your other functions. We suspect that it's a cerebellum function as the cerebellum is very involved in these areas. Over the last couple of years, I have also done a bit of work on developing a new scale, for detecting fear avoidance or activity avoidance. We used the Tampa Scale for kinesiophobia, which was originally developed for low back pain, and made it dystonia-specific. People have been using the Tampa Scale in pain for conditions like temporomandibular disorder and fibromyalgia; however, no one has ever used it in a movement disorder before. and I thought well if its activity avoidance and fear of movement, then why wouldn't you look at it in a movement disorder? It was about tapping into that whole selfperception of whether people change what they do on a daily basis for fear of triggering an attack of dystonia. Continues on page 7.
Heart & Soul Dystonia sufferer, Suzanne Bayliss, has put together a beautiful book of stories and poems of her personal experience with Dystonia. Suzanne has kindly donated books to the Brain Foundation for sale and all money goes to Dystonia research. Books are available for $10 each or you will receive one free with each $100 donation for Dystonia research.
Do you suffer from Parkinson’s? Do you live in Sydney? Would you like to try Pilates? Pilates Works in Cammeray is offering the first 5 lessons free for Parkinson’s sufferers. If you would like to see if this can help you, please phone Robyn Rix on (02) 8005 1565 or email on info@pilatesworks.com.au. This offer is also available for Dystonia sufferers. You’ll never know if you don’t give it a go!
Dystonia Awareness Month Don’t forget Dystonia Awareness Month in September For more information about Dystonia, visit australiandystoniasupportgroup.wordpress.com or email ADSG@live.com.au
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The Newsletter of the Brain Foundation
A Big DYSTONIA Thank you... to the members of Quota International Jimboomba, Queensland, for their very generous support of Dystonia research.
2015 Brain Awareness Week – March 16 to 22 With our banners flying, Brain Foundation took to the streets of Sydney with displays to raise awareness of who we are and what we do. After a very successful day in Queen Victoria Forecourt, we were privileged to join with Sylvia Liu's Fusion Culture Group for a display of brain training techniques and healthy body activities. Fusion Performers
Held at Customs House in Sydney, the event was part of the SCC Living in Harmony Festival 2015 and was free to attend. It was certainly action packed and we hope that the 160 people who came along gained some valuable insights. Our thanks to Dr Michael Valenzuela who spoke with the audience about Dementia and keeping your brain healthy and Prof. Qin Guo who spoke about the benefits of social interaction.
Sylvia and Gerald
Have you seen our new website?
We would love you to have a look. Like all new babies, there may be some teething problems and we would welcome your input.
We think it looks very contemporary!
Headache Australia Headache Awareness Week – September 14 to 21 During Headache Week 2015, the Brain Foundation will be inviting Headache Register members to a free public forum on Migraine Management. To be held in Brisbane, Sydney and Melbourne, each forum will commence at 6.30pm and aims to help you better understand your condition and the treatment options available to you.
Registrations are essential. Please check the Headache Australia website for further details.
Brisbane – Wednesday 16th – Dr Nicole Limberg, George Williams Hotel
Sydney – Monday 14th – Dr Bronwyn Jenkins, Kolling Institute, Royal North Shore Hospital
Register members will also be invited to join a series of Webinars on Migraine management.
Melbourne – Monday 14th – Assoc/Prof David Williams, Alfred Hospital
Appy? Nearly The redeveloped and improved iManage Migraine App is very close to being available for free for iOS and Android. This app, if used actively, will help you with your migraine management.
These are currently under development – so, look out for more information to follow via e-mail.
We will be taking our very popular Headache information desks to Federation Square in Melbourne on Tuesday 15th and Queen Victoria Forecourt in Sydney on Thursday 17th September. Come along and visit us.
At the time of going to print, we were about two weeks away. So have a look in the Apple Store or Google Play Store by mid-June and give it a go. The Brain Foundation cannot offer medical advice and we must stress the importance of discussing any issues you have with your medical practitioner.
Are you on the Headache Register? Our register members receive regular email updates of current information as we receive it. Your email address is required to receive information. Don’t miss out, join now! headacheaustralia.org.au
Winter 2015
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2015 Progress Reports Brain Foundation brings you the latest research findings from 2013 Grants. Two of these projects have applied for NHMRC (government) funding to further progress the initial results towards a better understanding for treatments in Stroke and Frontotemporal dementia.
Dendric spine alterations in TDP-43 aggregated Frontotemporal dementia: a novel therapeutic target 2013 Brain Foundation Grant
Chief Investigator: Dr Catherine Blizzard Frontotemporal dementia (FTD) has a prevalence second only to Alzheimer’s disease persons under the age of 65. And yet, relatively little is known about how pathogenic events lead to cognitive decline. FTD is caused by frontotemporal lobar degeneration (FTLD) that can be pathologically characterised by the cytoplasmic accumulation of aggregated proteins. One such protein is the transactive response DNA-binding protein 43 (TDP-43). There is increasing evidence that early synaptic alterations play a key role in many neurodegenerative diseases. Recent studies have shown that, in addition to its’ localisation to the nucleus and pathologically in the cytoplasm, TDP-43 is also localised within somatodendritic spines of hippocampal neurons, where it has been shown to act as an upstream regulator of spine turnover and homeostasis. These observations, in conjunction with our preliminary evidence of synaptic scaffolding proteins being misprocessed
in the TDP-43 A315T biological model of FTLD, open up a new potential route by which TDP-43 can affect neuronal function and conversely be implicated in the pathogenesis of neurodegenerative diseases. Therefore we are investigating the novel hypothesis ‘mutant TDP-43 results in synaptic pathology, leading to impaired neuroplasticity and ALS’. To achieve this we have created a novel transgenic biological model cross, using the TDP-43A315T biological model of FTD, and yellow fluorescent protein (YFP) models. These models ubiquitously express YFP in subsets of motor neurons in the cortex, making them an ideal model to study synapse morphology. With this transgenic biological model we have created a complete tissue bank of YFP crossed TDP-43A315T positive and control brains over a time-course of disease and are currently characterising levels of synaptic proteins and postsynaptic spine densities and morphology. Immunohistochemistry directed at endogenous YFP and synaptic markers
was performed on tissue from TDP43A315T models crossed with YFP-H models (P30 n = 5, P90 n =5) and in YFP-H litter matched controls (P30 n = 5, P90 n = 5). Confocal microscopy with subsequent image analysis was used to quantify YFP-H expressing layer V pyramidal neurons, pre-synaptic punctum and basal and apical dendritic spines in the motor and somatosensory cortices. There was no significant difference in the number of YFP-expressing pyramidal neurons in either the motor or somatosensory cortices between TDP43A315T x YFP-H models and YFP-H controls at 30 days (p > 0.05, twoway ANOVA with Bonferroni post-hoc test). There was however, a significant reduction in pyramidal neurons of the motor cortex in TDP-43A315T x YFP-H models compared to controls at 90 days, and in comparison to the motor cortex of TDP-43A315T x YFP-H models at 30 days. No significant changes were identified in pre-synaptic punctum levels at either time point (p > 0.05, two ANOVA
with Bonferroni post-hoc text). At 30 days, there were no significant differences in spine density between TDP-43A315T x YFP-H models and controls; however, in TDP-43A315T x YFP-H models at 90 days there were significant reductions in the spine density of motor basal and apical dendrites, and of somatosensory apical dendrites, in comparison to YFP-H controls. Furthermore we are currently in the process of establishing the 2PLSM live imaging platform in this novel mouse cross that will enable us to determine a precise time-course of synaptic alterations, pin-pointing the earliest synaptic events occurring prior to cell loss. Our findings, which form the backbone of a 2016 NHMRC project grant application, suggest post-synaptic dysfunction may be an early-occurring event in mutated TDP-43 pathology, occurring prior to neuronal loss. Understanding the role that TDP-43 plays in synaptic dysfunction may reveal new therapeutic windows for intervention in TDP-43 proteinopathies.
Targeting astrogliosis and brain stimulation after stroke to promote plasticity and functional recovery 2013 Brain Foundation Grant
Chief Investigator: Dr Carli Roulston Stroke often results in permanent brain damage which is ultimately due to a failure of nerve cells to re-grow across the injury site. Although the brain generates new stem cells in response to injury very few of these cells end up replacing damaged circuitry. Indeed, studies now show that the majority of migrating stem cells after stroke differentiate into astrocytes that become rapidly activated and contribute further to glial scar formation. Over activation of pre-existing astrocytes also disrupts neuronal signalling through reduced neurotransmitter turnover and energy transfer. We therefore hypothesised that targeting over-activation of astrocytes to reduce the glial scar would facilitate recovery of neuronal pathways affected by stroke.
Our first study explored the potential effect of delayed treatment with the Rho-kinase inhibitor, fasudil, on reducing astrocyte reactivity after stroke. These studies were performed by an honours student, Ms Ellie Phillips, supervised by Dr Carli Roulston, as part of the Biomedical Science degree at the University of Melbourne. Stroke was induced through application of the potent vasoconstrictor Endothelin-1 (60mol in 3µL saline) to constrict the middle cerebral artery in conscious male hooded Wistar models. Fasudil treatment was delayed until 3 days after stroke (50 mg/kg, intraperitoneal injections, daily) with vehicle (saline) and sham controls. Models were treated for 28 days (n=9 per treatment group), over which time functional outcomes were assessed
using various tests including the neurological deficit score, cylinder test, tape test and staircase test. After 28 days histological analysis of brain sections were conducted to observe the effect of fasudil treatment on astrocytes and other brain remodeling events. A smaller cohort (n=5 per treatment group) was recovered to 14 days and quantitative proteomics conducted using stable isotope dimethyl labelling in order to assess early changes in protein expression that may lead to functional recovery. Stroke resulted in observable brain injury in all models with no difference in infarct size detected between treatment groups. Neurological deficits were detected in all groups after stroke and were significantly recovered following treatment with
Fasudil, in comparison to vehicle controls. Given that treatment with Fasudil was delayed until after damage had occurred, the results of this study suggest that Fasudil can promote functional recovery in the absence of neuroprotection. Further histological analysis confirmed that fasudil treatment significantly reduced the number of astrocytes present in the damaged striatum and cortex and astrocytes that were detected showed a less reactive morphology similar to that of trophic astrocytes. Since recovery to the contralateral forepaw was rapidly observed upon treatment, we suggest that the effects of Fasudil are likely mediated through restored neurotransmission in surviving pathways, rather than axonal regeneration or remodelling. As such we have identified a new target for Fasudil, To top of page 5
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The Newsletter of the Brain Foundation
astrocytes, to retain neuronal-astrocyte metabolic coupling for restoration of neurotransmission. Quantitative proteomic analysis revealed that Fasudil treatment resulted in changes in protein expression levels. The most significant change was the up-regulation of dihydrolipoyllysineresidue succinyltransferase (DLST) following Fasudil treatment (12.29 ± 4.48 fold compared to vehicle). As an important component of the tricarboxylic acid cycle, DLST up-regulation may help astrocytes to maintain energy supplies, thereby allowing them to maintain neurotransmission without morphological transition into a diffuse, scar forming astrocyte. The results of this study support the use of Fasudil to promote post-stroke recovery through reduced astrocyte activation for
retained astrocyte support. Treatments that reactivate the depressed brain after stroke: Parallel to the above studies, we also hypothesized that direct stimulation of the stroke affected brain might also promote recovery of signalling pathways interrupted by stroke. Loss of electrical activity in otherwise structurally intact pathways now more accurately accounts for clinical findings and strategies that target this pathology represent an approach likely to enhance brain rescue and be accessible to a broader patient population. The use of electrical brain stimulation to treat stroke is an emerging concept. This study therefore explored the use of a minimally invasive epdidural device implanted over the biological model motor cortex to promote recovery after stroke.
Following endothelin-1 induced stroke and neurological screening in conscious models 2 separate groups (n=5 each) underwent either stimulation at functional threshold (6hr/day), or no-stimulation (where the stimulator is implanted but not turned on) for 5 days. Neurological outcome was assessed in all groups using a neurological deficit score and postural support cylinder test. After 5 days of stimulation immunohistochemical analysis was conducted to observe the effects on brain pathology. Epidural stimulation of the model motor cortex commencing 3 days after stroke promoted recovery of neurological deficits within 5 days (n=5). This is a marked improvement compared to reports using externalised devices and models without stimulation showed no evidence of recovery over the same period.
Stimulation resulted in accelerated angiogenesis within the damaged cortex in comparison to non-stimulated controls. Stimulation also altered the astrocyte response to stroke. Over activation of astrocytes into a diffuse morphology appeared to be reduced with epidural stimulation which is similar to that reported with deep brain stimulation. Epidural stimulation resulted in activation of astrocytes with a stellated morphology with spindly, elaborate processes extending outwards into the brain. Importantly astrocytes within the cortex retained end feet connections with blood vessels to potentially support reversal of functional deficits via neurovascular recoupling. These results suggest that electrical stimulation to reactive the sleeping brain after stroke may importantly involve retained astrocyte support.
Identifying the transcriptional cause of Multiple System Atrophy 2013 Brain Foundation Grant
Chief Investigator: Dr Michael Janitz Multiple system atrophy (MSA) is defined as a sporadic neurodegenerative disease, with an onset in adult life characterized by progressive development with etiology of an underdetermined nature. It is clinically characterized by varying degrees of the features of Parkinson's disease (PD) such as shaking, rigidity, slowness of movement, and difficulty with walking, and autonomic disorders of the genitourinary system and cortex. MSA equally affects both men and women, primarily in their 50s; however, disease onset as early as age 30 has been diagnosed. The progression of disease is rapid, and patients are confined to bed within 5 years of symptom onset with death resulting within an average of 9 years. With 3 cases per 100,000 individuals, MSA is considered rare; however, its prevalence is similar to multiple sclerosis (MS) (2.5 per 100,000) and motor neuron disease (1.5-2 per 100,000). We hypothesized that compared with PD, MSA has a fundamental dysregulation of transcription causing increased expression of α-synuclein protein. Therefore the aim of our proposal was to determine global transcriptome pattern in distinct regions of MSA brains using next-gene biological modelion sequencing and to validate expression patterns of genes determined as
specific to the molecular pathophysiology of MSA. We performed transcriptome sequencing of the brain tissue samples representing the superior frontal cortex derived from the multiple system atrophy (MSA) donors. We separately analysed grey (GM) and white matter (WM), of which major cellular components are neurons and oligodendrocytes, respectively. Since MSA-specific pathology is primary localized within the WM, affecting oligodendrocytes, through this sample selection we were able to assign changes in transcriptome profiles to the specific structures of the human cortex relevant to the disease pathology. We conducted the comparative transcriptome analysis in two dimensions. First, we considered the role of oligodendrocytes in MSA pathology and analyzed differences between the GM and WM transcriptomes within the MSA sample set. Second, we performed a pairwise analysis of GM and WM between MSA and control samples to capture fundamental changes in gene expression patterns resulting from neurodegenerative processes in each tissue type. Differential, genome-wide gene expression analysis revealed that MSA WM shows strongly elevated expression levels of haemoglobin genes (HBA1, HBA2 and HBB). Haemoglobin is the largest source of peripheral iron in the human body, and it may play a role in iron homeostasis throughout the brain. Disrupted iron
homeostasis has long been associated with various neurodegenerative disorders. It has been demonstrated that high levels of iron correlate with regions of neurodegeneration in both MSA and PD. High iron levels may also promote oxidative stress, alter myelin synthesis, increase the aggregation of α-synuclein and cause neuronal death. The selection of frontal WM with limited MSA-specific damage in our study further supports that such increases in haemoglobin levels may occur prior to neuronal loss. The correlation among iron, haemoglobin and neurodegeneration is further supported by the finding that high levels of α-synuclein are present in blood, specifically in red blood cells. Further, human histocompatibility complex class I genes including HLA-A, HLA-B and HLA-C, that relate to immune function, were all expressed at higher levels in control WM compared with MSA WM. These genes encode cell surface proteins that are constitutively expressed on microglia and endothelial cells in the brain and can be up-regulated in all brain cells in response to an immune challenge. Such reduced expression of HLA cell surface proteins in MSA WM may suggest a reduction in WMspecific immune function that could relate to the documented reduced involvement of inflammatory microglia in the progression of MSA degeneration. We also discovered a number of novel long intervening non-coding RNAs (lincRNAs) which were differentially expressed
between GM and WM in MSA cortical tissue. Interestingly, the top 10 up-regulated genes in GM included 4 un-annotated genes that satisfied the criteria for lincRNAs. The top 10 up-regulated genes in WM included 9 un-annotated genes that fulfilled the criteria for lincRNAs. Thus differential expression of lincRNAs suggests a strong regulatory component is involved in MSAspecific neurodegeneration. Taken together the results of this project contribute to our further understanding of the MSA pathology, in particular in the early stages of the neurodegenerative process. Of note, the outcomes of this project have been presented in three recent publications from Dr Janitz’s laboratory (Mills et al. 2014; Chen et al. 2015; Mills et al. 2015). Hypothesis vs Findings As we determined using RNA-Seq technology, the levels of α-synuclein gene (SNCA) expression were only moderately elevated in the MSA tissues. In contrast to our working hypothesis we conclude that despite an accumulation of α-synuclein aggregates, the levels of SNCA transcript remain largely unchanged in MSA. However utilization of a genome-wide approach to investigate the transcriptome perturbation in the course of MSA led us to discovery of new biological pathways which are affected in early stages of the disease progression. We have also been surprised by a high number of differentially expressed lincRNAs in the MSA brain. See website for complete reports Winter 2015
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Fabulous Fundraisers It would be remiss of us not to acknowledge the great contribution Carrie Bickmore has made to Brain Tumour Awareness with her beanies for brain cancer campaign. Your donations to this area of research are gratefully received.
#beanie
Beanies – a most stylish winter accessory Adelaide Hairdresser, Simon Lumsden has had a difficult couple of years. A wonderful friend had a fall and passed away as a result of a Brain Injury. Then, a client’s son, Dan, was diagnosed with a Brain Tumour and very soon after, another friend was diagnosed with an AVM. As if that wasn’t enough, another family member has spinal damage from an accident. This is enough to make your hair fall out…well in Simon’s case, he decided to shave it all off to help raise awareness and fund some research. Raising just shy of $6000, our thanks to all who supported the cause. So, I guess now, that beanie will be required!
Second thoughts Simon?
Simon and Dan – double trouble
What do 140 kilometres, 3 days and 1 wheelbarrow have in common? Well, they all go together for research into Brain Injury!
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The Newsletter of the Brain Foundation
A very sincere thank you to Cheryl Doyle and her family, who held a wonderful Christmas Cocktail Party to raise funds for Brain Tumour research. Held in memory of her late husband, Dr John Doyle, the family raised well in excess of $14,000. This is Cheryl's second very successful event for Glioblastoma Brain Cancer research. Thank you Cheryl, Ashley, Hailey, JK and Gregory.
Cheryl Doyle and her family
Are you thinking what I’m thinking? This is a very long way – 264kms to be exact. Aunty Ann and sister and team organiser, Rhegan
Why? Callum’s sister was diagnosed with a Tumour and thankfully the removal has been successful. Her fight has inspired Callum to action because not everyone is so lucky. So, donning a surf lifesaving cap, Callum is raising funds.
Eboni, Sharon and Jaimen, Zanes girlfriend, mother and sister
54 teams competed, although I think just finishing was competition enough. Averaging 12 km per hour, there were plenty of sore muscles and massages required. The team raised an amazing $6300. I’m sure Zane would be very proud of the achievements of all them. A special thank you to Uniformlink and Avis who supported the team in this event.
Beanies – make mine Black Tie
In January 2016, a very intrepid Callum Smith of Melbourne is planning to paddle around Port Phillip Bay.
Feeling the enormous loss of their son and brother, the family of Zane Hartwig wanted to help fund research so that others may not have to face the same devastating loss.
Covering 140kms, from Mareeba to Chillagoe, the 3 day Great Wheelbarrow Race is a big event.
sforb
No beanie required
At the end of 2014, the community of Cairns lost a wonderful young man – taken from them by a Traumatic Brain Injury.
So, wheelbarrows it was, and Team Zane was born.
ou! Thraaninkcayncer
You can support him via our website or via mycause.com.au, Port Phillip Bay Paddle.
2015 Tamworth Fair To be held on Sunday, November 22. Your support of this wonderful event is appreciated. Niece Skylah gets in on the act
Exercise your brain An active brain is your best asset. Use it every day for best results This month we have a set of the very popular Sudoku puzzles. Try your luck. Remember, don’t start at a level which is too hard. You have better success building up your skills. Our thanks as always go to Brain Food Factory. To keep your brain in optimum shape, you can subscribe to the free monthly puzzles at brainfoodfactory.com
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Solutions on back page
Deconstructing Dystonia cont... How widespread is the use of TMS? Is it being utilised clinically for patients with dystonia? It's really a research tool at the moment; there are only a few physiotherapists around the world trained in its use, and there's a handful in Australia. At the moment you have to do specialised training, which most people do as part of a PhD. Most of the work has been done in the area of stroke rehabilitation and it's seen as more of an adjunct to therapy. What areas would you like to see researched further? One of the things that holds dystonia back, in terms of treatment from doctors and neurologists, as well as physiotherapists, is we don't really understand the pathophysiology properly. It's not as clear-cut as Parkinson's. Although the basal ganglia are probably involved in dystonia, no one has ever been able to find any evidence of neuron degeneration. Over the last five years or so, evidence has emerged that the cerebellum is quite strongly involved in the pathophysiology, probably in combination with the basal ganglia; those two areas of the brain talk to each other quite closely but we don't know if the cerebellum is the primary problem and the basal ganglia is secondary or whether it's the other way round. Once we understand the pathophysiology and know where in the brain the dysfunction is, then we can target our therapies to that dysfunction. We need lots of evidence-based physiotherapy to know exactly what sort of interventions work the best for these people. What treatments are currently available for dystonia patients? At the moment, the only treatment available is botulinum toxin injections, which are painful. They have to be repeated every three months, and quite often they only really work well for about the middle four weeks of the three-month cycle.
The injections don't address the cause of the dystonia; they just treat the symptoms and they seem to become less effective over time. As the muscles get more atrophied, it is harder to get the injection into the affected muscles and because there are so many muscles in the neck, it's difficult to find the ones that are causing the dystonia. For the people who can't have them or don't want them, there's not a lot else on offer, which is why we are finding the brain stimulation studies quite exciting: it's not going to be a cure but it might offer people an alternative to the injections or something they can have alongside the injections to make them more effective. We are having a go at trying to treat the brain, which might be the cause of dystonia, rather than just treating it symptomatically. Should physiotherapists be playing a greater role in the treatment of patients with dystonia, to target the secondary conditions that accompany the disorder? That's the interesting thing. You would think so, and really, as physiotherapists, we should be a bit offended that we aren't. They [patients] go to the neurologist and then they go home, and sometimes they find their way to physiotherapists through special interest groups. But they are not routinely referred. They are not getting the strength training or the mobility training or any kind of rehabilitation and support. Botulinum toxin injections make their muscles quite weak. As physiotherapists, we can help them to strengthen their muscles. They often have a lot of postural problems. Because their neck is in a twisted position they end up twisting their spines to compensate so they get problems in other places. It's about reducing those secondary dysfunctions that arise from compensation of the head position.
A lot of it too, with physiotherapy, can be just support for people. Because they only see neurologists, they don't have much of chance to talk to people about their condition. We feel-and this is from international collaborations that I have with other therapists who are also neuroscientiststhat if the botulinum toxin injections were combined with physiotherapy, we could extend the time that they have to have these injections by working on the motor control aspect while the botulinum is working on those dystonic muscles; and then we might have a chance at making a positive change in the brain, and therefore in their symptoms. But until we provide evidence that what we do is useful, we're not going to have much luck, and unless we do a strong campaign, as a profession, to get these people in our clinics, they are not going to come. How would a better understanding of dystonia improve health practitioners' treatment of the disorder? We need to highlight it, first of all, as an issue, and educate therapists as well as the rest of the health profession that dystonia is a problem. It's the third most common movement disorder worldwide, so we should know about it. One of the problems these people face is every time they go somewhere they have got to explain what their condition is. They find themselves going to newly trained doctors and physiotherapists who have never heard of dystonia. If they've got to explain what their condition is, it just makes life that much harder for them. This is a condition we should know more about ... we should be owning it ... treating and researching it. They are a population that need someone to get on their bandwagon, and there's so much more we could be doing as a profession to help them.
Winter 2015
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Go Fundraise: Karen Payne (below), Hugh O’Reilly and Team Brainiacs, Christina CardilloZalio, VirginiaScott, Team Zane.
You can set up your individual page using Go Fundraise, My Cause or Everyday Hero and then let your friends, family and workmates know. Updating everyone is made simple. Call our office, we are happy to support you.
My Cause: Anthea Simmons, Clare Hines, Saoirse O’Sullivan, Luke McIlwrath. Everyday Hero: Callan Boslem, Carol Gilmour, Tiffany Chan, Katie Burgess.
In Memorium To all the families who have lost a loved one, a very sincere ‘thank you’ for the donations in their memory: Joyce HALL Zane HARTWIG Anh To QUACH Ouriania CHRISTOU
Calling all Party Zombies
It’s FUN RUN time again!
Margaret Anne SEDSMAN
Before we know it, it will be the annual party time for Zombies. Dress up or dress down, but make sure you come along to enjoy the spectacle.
For those enthusiastic runners, the City 2 Surf and Bridge to Brisbane entries are now open.
Rex WALSH
There are many community events held in all major areas. Have a look and get involved. Or, if someone you know is planning to take part, let them know we are a good cause for them to support. Brain disease can affect anyone at any time.
Look out for walks in Brisbane, Cairns, Canberra, Perth, Townsville & Sydney. Or, give our office a call for the dates.
Regular Giving Would making small, regular donations suit you better than one bigger donation per year? Perhaps you should think about making a regular monthly or quarterly donation. Contact our office or download a form and we will do the rest for you.
Workplace Giving is an easy alternative and your company may even match your donation. Speak to your paymaster for further information.
Estate Planning and Bequests: Our benefactor, Australian Executor Trustees offers reduced rates for Brain Foundation supporters. For more information, please call Gerald in our office on 1300 886 660.
Brain Foundation is registered with Go Fundraise, My Cause and Everyday Hero, so it is easy to fundraise to support research. Or, you can create your own fundraising page via the Brain Foundation web site. If you get a team together, give our office a call so we can send our lime green caps for all to wear.
Iris JOHNS Renee SHEEDY Noel CLIFTON Rod BOURKE Georgia BOURKE Bobby BALLANTYNE Glen HOWSE Pam MORGAN Nick PSYHOGIOS Carmela LENTINI Christopher WILLIAMS Vittoria ZUCCARINI Mark COLYS Arthur Graham SPOONER John Wasley SMITH Judith Anne WATERMAN Pauline Shirley RUCH Elizabeth RIGG
In Celebration We would like to send our best wishes and congratulations to the following couples who donated ’In Celebration’ of their wedding: Michael HALMAGYI & Gulden AKDAL
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Kieran & Amanda CHOY
Thanks to the following companies for their support:
Thank you for supporting brain research through the Brain Foundation To make a donation please visit our website brainfoundation.org.au/donate or use the donation form on the letter enclosed.
Caroline TRUEMAN & David BUTCHER