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Cornwall. She also serves as director of geriatric psychiatry at the University of Ottawa. She has spent her career not in a research laboratory but in what she describes as the "trenches" of dementia treatment. Her work focuses on treating the depression, aggression and inappropriate behaviours that often accompany dementia. Ninety per cent of people with dementia will have behavioural problems, she says, so addressing those issues can significantly decrease the distress of patients and caregivers. Dr. Rivard is a tireless advocate for people, like Jeffrey, who suffer from Alzheimer's disease. She has played a key role in improving the education that Ontario doctors and medical students receive about dementia: how to diagnose it and how to treat it. She has worked on the province's Alzheimer's strategy and is a member of a group planning how to meet the future health care needs of seniors in the region. In 2003, she was the inaugural recipient of the Canadian Academy of Geriatric Psychiatry's award for outstanding contributions to the field. It is a fulsome career that has afforded her an intimate understanding of Alzheimer's disease. Indeed, through her 30 years of experience, it is possible to glimpse the arc of Alzheimer's and begin to understand how the scientific view of this disease has shifted over the past decades. There has been much heartbreak in her casework over that time. But, more than ever now, there is hope. When Dr. Rivard began her career at the Royal Ottawa Hospital in 1979, Alzheimer's disease was not a household term. Other than some basics, doctors knew little about the disease and how it differed from normal aging. "When I was 30 years old, we were still talking about senility and expecting that when I got old I would be senile, " Dr. Rivard says. "We were not making the distinction between what is normal aging and what is Alzheimer's disease. So we were not diagnosing." Diagnosis came late in the illness, if at all; there was no effective treatment. "People were saying this is something we can't do anything about." Today, the disease is part of the common lexicon. People regularly refer to their "Alzheimer's moments" when they misplace their keys or forget an anniversary. But there is also an understanding that Alzheimer's disease involves much more than memory lapses. The number of Alzheimer's patients in Canada has grown alongside the country's aging population. About eight per cent of people older than 65 suffer from Alzheimer's disease or another kind of dementia. "It touches all of us now, " Dr. Rivard says. "It seems everyone has a family member with Alzheimer's disease, or knows someone who has it." Today, doctors are able to diagnose the disease early and accurately in more than 90 per cent of cases. Researchers also understand a great deal more about how Alzheimer's disease develops, how it affects brain cells and how each of its stages will progressively attack more of an individual's brain functions. For a century, scientists have been able to identify Alzheimer's as a disease by the plaques and tangles found on autopsied brains. In 1984, researchers identified betaamyloid, a protein fragment, as the culprit behind the plaque that forms between nerve cells in the brain. In the early 1990s, they discovered that mutations of another protein, called tau, produce the tangles -- under a microscope, they look like spidery threads -- that destroy neurons from within. Later, they showed how the protein-fuelled plaques and tangles weaken and kill those nerve cells in the brain. What makes Alzheimer's disease so insidious is that those plaques and tangles may be growing in the brain for many years before there are symptoms. It means that by the time a diagnosis is made the brain is already damaged -- it's too late. Still, there are treatments that will temporarily slow the damage. In the mid-1990s, a family of drugs called cholinesterase inhibitors were developed. These drugs -- the brand names are Aricept, Reminyll and Exelon -- cannot stop the progression of the disease, but do slow the symptoms in the short term. The drugs work by increasing the level of a brain chemical called acetylcholine. "If you boost acetylcholine, it allows and hytrin!

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TP 096 PROLONGED GRAFT ISCHAEMIC TIME DOES NOT REDUCE SURVIVAL AFTER LUNG TRANSPLANTATION IN AUSTRALIA Glanville AR, Aboyoun C, Plit M, Malouf MA TP 097 DIRECT IMMUNOFLUORESCENCE ON NASOPHARYNGEAL SWABS EFFECTIVELY IDENTIFIES COMMUNITY ACQUIRED VIRAL INFECTIONS AFTER LUNG TRANSPLANTATION Havryk AP, Aboyoun C, Murphy KM, Malouf MA, Plit M, Glanville AR TP 098 CYTOMEGALOVIRUS PCR TESTING HAS A HIGH NEGATIVE PREDICTIVE VALUE FOR TISSUE INFECTION AFTER LUNG TRANSPLANTATION Murphy KM, Pearson R, Aboyoun C, Plit M, Malouf MA, Glanville AR TP 099 GASTRO-OESOPHAGEAL REFLUX GOR ; : A SIGNIFICANT PROBLEM IN CF BEFORE AND AFTER LUNG TRANSPLANTATION Button B, Kotsimbos T, Sherburn M, Chase J, Wilson J TP 100 DIFFERENTIAL RATES OF APOPTOSIS IN BAL AND BLOOD OF LUNG TRANSPLANT PATIENTS Hodge SJ, Hodge GL, Reynolds PN, Holmes MD TP 101 PLASMA INTERLEUKIN 15 AND GRANZYME B IN LUNG TRANSPLANT RECIPIENTS USEFUL REJECTION MARKERS? Liew C, Hodge SJ, McNamara T, Hodge G, Holmes MD, Reynolds PN TP 102 INITIAL INCREASE OF BASEMENT MEMBRANE THICKNESS IN AIRWAY WALLS POST TRANSPLANT SEEMS NOT TO BE A RISK FACTOR OF FUTURE BRONCHIOLITIS OBLITERANS SYNDROME Law L, Zheng L, Orside B, Levvey B, Oto T, Kotsimbos ATC, Snell GI, Williams TJ TP 103 CASE REPORT: SHORT-TERM HIGH DOSE CORTICOSTEROID THERAPY AS A RISK FACTOR FOR PNEUMOCYSTIS CARINII PNEUMONIA Stone E, Murphy K, Moore J, Cook R TP 104 VENOUS THROMBOEMBOLISM PROPHYLAXIS IN THE THORACIC INPATIENT POPULATION: AN AUDIT OF CURRENT PRACTICE Stone E, Reynolds P, Harris B, Dennis C TP 105 THE HUNTER PULMONARY EMBOLISM DIAGNOSIS STUDY: A PROGRESS REPORT Hamilton S, Hensley M, Thomas P, Rogers K, Lewis G, Allen L, Viswanathan S, Soans B, Holt L, Abel C, Chan V, Nicoll A TP 106 SPECT VENTILATION PERFUSION V Q ; AND CTPA: CO-LOCALISATION OF SUSPECTED PULMONARY EMBOLI PE ; IN FUSION IMAGES Harris BE, Bailey D, Roach P, King G TP 107 PLEURAL EFFUSION IN PATIENTS WITH PULMONARY EMBOLISM DETECTED BY CT PULMONARY ANGIOGRAPHY Yap E, Anderson G, Donald J, Wong C, Lee YCG, Sivakumaran P TP 108 IL D-DIMER OUTPERFORMS PRETEST SCORING SYSTEMS IN ASSESSMENT OF POSSIBLE COMMUNITY PULMONARY EMBOLISM Beckert L, Ardagh M, Lawson R, Taylor C, Than M TP 109 DEFINING THE ROLE OF CTPA'S IN PATIENTS ADMITTED TO GENERAL MEDICINE. Recent studies ascribe risk factors to the increased incidence of nonspecific musculoskeletal spinal disorders table 1 ; . Detailed analysis of musculoskeletal disorders in the workplace has led to the conclusion that there is a moderate to strong association between nonspecific spinal disorders and heavy physical load. For pain in the lumbosacral spine region, these physical parameters include exposure to activities which involve manual material handling, load moment, frequent bending and twisting, heavy physical work, and whole body vibration. For the pain in the cervical spine region, the most common risk factors are repetitive movements of the neck and arm s ; , static posture and segmental vibration through hand-held tools.Work-related psychosocial factors associated with spinal disorders include rapid work pace, monotonous work, low job satisfaction, low decision latitude, and job stress. Other characteristics affecting the susceptibility to spinal disorders include age, gender, Body Mass Index, and individual psychosocial factors. There may be a genetic factor involved in spinal disorders involving the disk. Studies show a positive family history as a risk factor for disk herniation. The exact cause of this predisposition is not known and could be a result of congenital spinal abnormalities or a small vertebral canal, which would increase sensitivity to mechanical stress on the back, because reminyl 16 mg.
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