Sharon Yardley, RN Clinical
Coordinator, Vancouver Hospital
Movement Disorders Clinic

Co-author
Susan Calne, RN
Coordinator Neurodegenerative
Disorders Centre

Introduction
I work at the Neurodegenerative Disorder Centre at the University of British Columbia, where we currently care for more than 1,500 patients with Parkinson's disease (PD). I work with four neurologists, all of whom have subspecialty training in PD, and on a part-time basis I also have the help of one other nurse. My role as the clinic co-ordinator, is to provide counselling and education to new patients, and as their disease progresses, to continue counselling these patients on an outpatient basis. By providing the patients with knowledge and support, we seek to optimize their quality of life and their independence.¹

The clinical co-ordinator focuses primarily on the patients, and provides them with information about PD, the emotional and employment issues that may arise during the course of the illness, and changes that will occur in their lifestyle. Another important function is to provide the patients with education about pharmaceutical treatment and monitoring services, and to support them as they begin antiparkinson therapy, documenting changes in their symptoms and any problems that occur between visits.

Drugs, Toxins and Pugilism May All Lead to PD-Like Symptoms

D'Arcy L. Little, MD, CCFP
Director of Medical Education
York Community Services,
Toronto, ON

Introduction
Diagnosing a patient with Parkinson's disease might, at first, seem to be straightforward. In some cases, a medical student can make the diagnosis from across a room. However, fully one quarter of the diagnoses of idiopathic Parkinson's, which were made clinically by specialists, were found upon pathological examination to be some other disease.^1,2,3 This figure is even higher in situations where the diagnosis was made in the early stages of the disease, by a non-specialist.³ Given that the list of conditions in the differential diagnosis of Parkinson's is vast, and the diagnosis is essentially a clinical one made by the process of elimination or exclusion, the clinician needs a solid approach when considering a diagnosis of this illness. The purpose of this review is to itemize an approach to the exclusion of cases of secondary parkinsonism, in the diagnosis of idiopathic Parkinson's disease (See Figure 1: Approach to Diagnosis of Parkinsonism). Table 1 lists clues that suggest a diagnosis of secondary parkinsonism.

It is well known that many elderly individuals have difficulty sleeping, and it is also known that aging is associated with a decrease in growth hormone (GH) levels. Changes in sleep patterns drastically affect endocrine function, especially pituitary-dependent hormonal release, which may impact on nighttime levels of GH. An interesting question then, is whether the age-related decrease in the quality of sleep is responsible for the age-related decline in GH hormone secretion or, alternatively, whether the reverse is true and the age-related decline in GH secretion may be responsible for the age-related changes in sleep patterns. A recent study published in the Journal of American Medical Association has taken a step towards determining this relationship, by closely examining the correlation between various stages of sleep and levels of GH, in healthy men between 16 and 83 years of age. The association between the two is striking. Not only does it raise the possibility of using GH supplementation to conquer yet another marker of biological aging--reduced sleep--but it also presents sleep enhancement as a potential way of increasing GH levels.

Previous studies have shown that aging is associated with increases in the number and duration of awakenings during the night and decreases in the amount of slow-wave (SW) sleep. There is also a decrease in the amount of rapid eye movement sleep (REM) but this change is moderate by comparison. This earlier data was based on a comparison of two age groups young and aged persons.

Nadège Chéry, PhD
Medical Writer/Consultant,
Snell Medical Communication Inc.
Montreal, Qc

The prescription of medications is among the most frequent and the most reliable forms of therapeutic strategy that physicians use for the treatment of patients with a variety of medical disorders.¹ Unfortunately, many of these medications also produce side effects, especially in the geriatric population,¹ some of which may be mild and relatively tolerable by most patients, and others, such as dyskinetic reactions, which are considered harmful.^2,10 Drug-induced movement disorders represent an important iatrogenic condition that is occasionally encountered in clinical practice.² These potentially disabling movement disorders are involuntary, they appear to be idiosyncratic extensions of the expected action of the drug and they are known to particularly affect the elderly patient.^2-6 Among the devastating consequences of these disorders are involuntary movements, which may contribute to falls and fractures in the elderly, and social isolation, which can result from the limited mobility of an elderly individual.^4,7

Nonetheless, movement disorders are often reversible; the withdrawal of the offending drug(s) usually leads to the alleviation of symptoms.³ Unfortunately, in some cases, discontinuing the offending drug may not be feasible.

An Interview with Dr. Caleb Finch

Kimby N. Barton, MSc
Associate Editor,
Geriatrics & Aging

This month we are pleased to present, as part of our Biology of Aging series, an interview with Dr. Caleb Finch, a world-renowned gerontologist. Dr. Finch has received most of the major awards in biogerontology, and since 1984, has directed the US National Institute of Aging funded, Alzheimer Disease Research Center. Probably one of Dr. Finch's most significant discoveries was that the brain makes messenger RNAs (mRNAs) for several inflammatory mediators, known as complement factors, that were previously believed to be absent from the brain. In addition, he disproved a longstanding belief that the activity of mRNAs globally decreases with increasing age.

Dr. Finch's current research is focused on the molecular and cellular mechanisms of aging in the brain, and the selectivity of neurodegeneration. His research team is analyzing the transcriptional control, in the brain, of complement factors and other mRNAs that are known to change during aging and with neurodegenerative disease. I was afforded the opportunity to ask Dr. Finch some questions regarding his recent research and major developments in the field of aging.

New Cognitive Enhancers Prevent Breakdown of Acetylcholine

Karl Farcnik, BSc, MD, FRCPC
Michelle Persyko, Psy.D, C.Psych
Psychiatrist,
Division of Geriatric Psychiatry,
University Toronto
Part-time staff,
Toronto Western Hospital

Introduction
Acetylcholinesterase (AchE) inhibitors have now become the medications of choice for first-line therapy in the treatment of Alzheimer's Disease (AD).¹ In Canada, there are currently only two drugs that have been approved for the treatment of mild to moderate Alzheimer's Disease; these are donepezil (Aricept)² and rivastigmine (Exelon).³ They have greater central specificity, and a much more favourable side effect profile, than do earlier AchE inhibitors such as tacrine (Cognex). Their role in the treatment of this disease is significant, since research is showing that they impact not only on the cognitive deficits associated with AD, but also help to preserve activities of daily living (ADL) and decrease behavioural problems. Cognition and ADL are both areas that are affected by Alzheimer's disease.⁴ Administration of these medications has been shown to be beneficial throughout the disease process. This paper describes donepezil and also rivastigmine, which is the newest AchE inhibitor that has been approved in Canada.

The history of the use of pharmaceuticals to alleviate the symptoms of Parkinson's disease (PD) began 125 years ago, when belladonna alkaloids were first used in an attempt to control severe drooling in patients suffering from PD. These alkaloids possess anticholinergic activity, and unexpectedly, they alleviated other characteristic symptoms of PD, which include tremor, rigidity, akinesia and postural instability. However, it was not until 1958 that researchers discovered the presence of high levels of dopamine in the striatum of the brain and showed that the dopamine precursor (levodopa or L-dopa) reversed the tranquillization and parkinsonian-like motor impairments induced by treatment with reserpine. This set the stage for the development of the first real pharmacotherapy for treatment of PD.

Sanjiv CC, DM,
Tsui JKC, MD, FRCPC
Neurodegenerative Disorders Centre,
University of British Columbia,
Vancouver, BC, Canada

Dopaminergic Agents
At present, there is no pharmacological cure for Parkinson's disease (PD) and only the symptoms of the disease can be treated. There is no firm evidence to support the notion that any drug has a neuroprotective action in PD; therefore, the mainstay of current drug therapy is the manipulation of the dopaminergic pathways.

Levodopa (L-DOPA)
L-dopa is the most commonly prescribed medication for the treatment of PD.

Janis Miyasaki, MD, FRCPC
Mount Sinai Hospital,
Movement Disorders

Each year Parkinson's disease (PD) affects 4.5-21 people out of every 100,000. The prevalence rate is 200/100,000 members of the population. As the population ages, the prevalence can be expected to increase since the risk of developing PD steadily increases with each decade of life.¹ The cardinal symptoms of PD are tremor, rigidity, akinesia and postural instability.² A patient is diagnosed with Parkinson's disease based on him/her having a history consistent with PD, and showing the clinical signs on examination. Therefore, the physician must be familiar with the classic appearance of each sign of PD and with the alternative diagnoses that are implied by any variance in symptoms.

Tremor
The tremor in PD is classically 3-5 Hz and is described as pill-rolling, due to the rhythmic opposition of the index finger and thumb. Tremor is seen at rest, however, in some cases it may only be seen if the patient is distracted by the use of manoeuvres such as mental arithmetic. While the patient is walking, the affected arm will often shake. Anxiety markedly increases the tremor, whereas it abates during sleep. Tremor may also be seen with postural maintenance or during a physical action. If the postural or kinetic component of the tremor is predominant, the physician should consider an enhanced physiologic tremor or essential tremor as the diagnosis.

Basal Ganglia Motor Circuit is Target Site for Surgical Intervention

Farooq I. Khan, MD,
Robert Chen, MBBChir, MSc, FRCPC
Movement Disorders Centre,
Division of Neurology,
Toronto Western Hospital,
University of Toronto

Parkinson's Disease (PD) was first described by James Parkinson in 1817, and is a neurodegenerative disease that is characterized by tremor, bradykinesia, rigidity and postural instability. It results from the degeneration of the dopaminergic neurons in the substantia nigra (pars compacta) causing alterations in the basal ganglia circuitry; this circuitry is responsible for modulating and facilitating motor function through the cerebral cortex. The evolution of the treatment for PD has relied on both pharmacological and surgical approaches, arguably the most important of which was the discovery of levodopa in the early 1960s. Since then a number of other pharmacological agents such as monoamine oxidase (MAO) inhibitors, catechol-O-methyltransferase (COMT) inhibitors, and dopamine agonists, have played a vital role in the amelioration of disability arising from this disease. Unfortunately, long term pharmacotherapy, especially with levodopa, has caused problems of its own, namely the occurrence of fluctuation and dyskinesia. For these and other reasons that will be discussed, surgery has offered a ray of hope to combat this eventually crippling disease.

In 1942, a young British flight surgeon, Ridley, made an outstanding discovery that was to shape the future of cataract treatment. Cataracts result from the clouding of the lens of the eye, which leads to blurred vision. As with the lens of a camera, the lens of the eye functions by focussing light rays onto the retina at the back of the eye, which then transmits this visual information to the brain. For the light to pass through and reach the retina, the lens must remain clear. Cataracts result when the natural lens of the eye becomes cloudy; they are not the product of a growth or the accumulation of film over the eye.

While examining injured fighter pilots, Ridley noted that when plastic slivers from the shattered windshield of an airplane cockpit entered the eye, some pilots had a severe reaction, whereas other pilots had no reaction at all. At the time, the accepted belief was that any foreign material entering the eye would cause a severe reaction until it was removed. Ridley wanted to understand why some pilots showed no reaction to the presence of a piece of plastic in their eye. Further investigation led him to realize that it was only the pilots of Spitfires who did not suffer any complications, whereas pilots flying all other British fighter planes--including captured German pilots flying Messerschmitts--were all severely affected. The young surgeon then discovered that Spitfire plastic came from a different company, ICI, that produced a type of plastic material, polymethyl methacrylate, which could be tolerated by the human eye.

When the war ended in 1945, Ridley turned his attention to cataract surgery. Treatment at the time involved removing the diseased cataract lens and giving the patient thick, heavy glasses that limited their peripheral vision and magnified objects by 30 %. Ridley decided that a better technique for cataract treatment would be to replace the human lens with a lens made of the plastic that he had discovered during the war. On 19 November 1949, at St. Thomas's Hospital in London, he performed the first lens implant on a cataract patient.

Today the treatment of cataracts still relies solely on surgical techniques; there is no medication or diet that can stop a cataract once it has begun to form. A cataract may develop rapidly over a period of a few months or it may grow very slowly over several years. Typically, this process only occurs in a single eye, although eventually, often after months or years, a cataract may develop in the second eye. Most cataracts are related to aging, although they may also be congenital, the result of a medical problem such as diabetes or of a trauma to the eye.

A cataract rarely causes damage if it is left in the eye, except in cases in which there is blurred vision. There are very rare cases, however, of cataracts, when left in the eye long past the stage of blindness, causing inflammation and glaucoma. With the current methods of removal, surgery can be performed successfully at any stage of cataract development.

The only treatment for a cataract is the removal of the cloudy lens. There are various methods of surgically removing a cataract, and the specialist must decide which method is most suitable for each individual patient. For a description of the three main surgical procedures that are available for cataract extraction, and a list of the advantages and disadvantages of these techniques, please see the full article by Dr. Marvin Kwitko on our web site at www.geriatricsandaging.ca.

Dr. Marvin Kwitko performed his first lens implant operation at Bellechasse Hospital in Montreal in 1967. In 1968 he joined St. Mary's Hospital, and under the former chief, Dr. Gaston Duclos, continued this work there. Dr. Kwitko has trained more than 350 surgeons from Canada, the U.S. and abroad. He is currently the Chief of Opthalmology at St. Mary's Hospital in Montreal and an Associate Professor of Ophthalmology at McGill University.