Advertisement

Advertisement

Articles

Depression in Idiopathic Parkinson’s Disease

Depression in Idiopathic Parkinson’s Disease

Teaser: 

Christopher Hyson MD, FRCPC, Clinical Fellow, Movement Disorders Program, London Health Sciences Centre, London, ON.

Mandar S Jog MD, FRCPC, Director, Movement Disorders Program, London Health Sciences Centre, London, ON.

Epidemiology
Idiopathic Parkinson's Disease (IPD), which results from degeneration of substantia nigra neurons, is characterized by the typical motor symptoms of rest tremor, rigidity, bradykinesia and postural instability. The estimated prevalence, which has been rising with the aging of the population, is 187/100,000 in the United States, with an annual incidence of 20/100,000. In addition to the well recognized motor disability, neuropsychiatric symptoms, such as depression, anxiety disorders and psychosis, are common, yet under-recognized in patients with IPD.1 It is, therefore, important that primary care physicians, internists and neurologists who care for patients with IPD be familiar with the occurrence and management of this important symptom.

Depression is the most common neuropsychiatric symptom seen in patients with IPD. It is estimated that approximately 40% of patients with IPD will experience depression at some point over the course of their illness. For 4-6% of these patients, the episode will meet the Diagnostic and Statistical Manual of Mental Disorders' (DSM-IV) definition of major depression. The remainder will meet the diagnostic criteria for minor depression.

What is ALS?

What is ALS?

Teaser: 

ALS, sometimes called Lou Gehrig's disease or Motor Neuron Disease (MND), is characterized by degeneration of a select group of nerve cells and pathways in the brain and spinal cord, leading to progressive paralysis of the muscles.

ALS involves the loss of motor nerve cells. The nerves affected are in the spinal cord and those that travel to the voluntary muscles, with weakness and wasting in the arms, legs and mouth, throat and respiratory system. The loss of nerve cells results in atrophy, or wasting of the muscles served by those cells.

Although symptoms of ALS usually present on one side of the body, both sides are involved and the effects usually become more symmetrical as the disorder progresses.

ALS does not discriminate. Anyone can get ALS--male or female of any race. It usually becomes evident as one approaches middle age. There is a very rare form transmitted from generation to generation and a very rare juvenile form.

ALS progresses relentlessly. There is no recovery or reversal and few plateaus; it is merely a rapid decline in motor capacity. For many, there is little impairment of the intellect and the senses remain intact.

Approximately 2000 Canadians live with ALS at any one time. Ninety percent of people with ALS will die within six years and the progression of the disease will remove them from society for much of that time. Two to three Canadians die of ALS every day.

What can be done?
Nation-wide, ALS clinics employ a team approach to the treatment of disease symptoms and assisting the person with ALS to live as fully as possible. Along with neurologists and other physicians, the team may include a physiatrist, respiratory therapist, occupational therapist, physiotherapist, dietitian, speech-language pathologist, social worker and pastoral care provider.

ALS Societies across the country make a valuable contribution, providing information and referral, access to specialized equipment in a timely manner, support groups for all concerned and advocacy for those affected by the disease.

These teams help those affected with ALS to make decisions that will assist in the management of ALS and to improve quality of life at each stage. Care-giving and caregiver support become vital as the person quickly progresses from independence to dependence.

ALS research in Canada is advancing toward treatment and a cure and research funding is increasing. For example, the ALS Society of Canada's participation in the Neuromuscular Research Partnership, working with the Muscular Dystrophy Association of Canada and the Canadian Institutes of Health Research, has funded nearly $6 million of research in the past two years.

Internationally respected, Canadian researchers are focussing on several areas including proteomics (the study of protein chemistry) to determine the cause of cell death and developing trials of potentially useful drug combinations.

These initiatives in stimulating research and provision of care will eventually result in increased longevity for those with ALS, with improved quality of life, and the hope of a cure for this devastating disease.

More information is available from the ALS Society of Canada site--www.als.ca.

Natural History of Long-Term Care Clients

Natural History of Long-Term Care Clients

Teaser: 

Madhuri Reddy, MD, Associate Editor, Geriatrics & Aging.

In order to effectively plan future long-term care (LTC) environments, it is important to ascertain the natural history of clients once placed in these environments. What, for instance, are the predictors of client mortality and the probability of a change in function, either to improve or deteriorate, once placed in a certain level of care? Environments need to be flexible and, most of all, promote independence and an enhanced quality of life.

Changes in Care Requirements Over Time
It is well established that the functional status of many nursing home (NH) clients improves after NH placement or after transitions between different levels of care. Some aspects of functional status (hygiene, dressing, grooming and transferring), as well as depressed mood, are likely to improve shortly after NH admission.1 One study of over 9,500 elderly clients admitted to a NH for at least 100 days found that 51.5% experienced a change in function during the first 90 days. This change usually represented an improvement rather than a decline. In fact, thirty-seven percent of this long-stay client sample was able to return home.2

Predictors of Mortality
Several studies have indicated that predictors of mortality in the elderly are increased age, male sex, poor physical status, poor social supports and poor cognitive functioning.3,4,5 Few studies, however, have investigated the predictors of mortality specific to the NH population.

Rehabilitation in the Elderly Stroke Patient

Rehabilitation in the Elderly Stroke Patient

Teaser: 

Robert W Teasell, MD, FRCPC, Professor and Chair-Chief, Department of Physical Medicine & Rehabilitation, St Joseph's Health Care, London, University of Western Ontario, London, ON.

Timothy J Doherty, MD, PhD, FRCPC, Assistant Professor, Department of Physical Medicine and Rehabilitation, The University of Western Ontario, London, ON.

Defining Stroke Rehabilitation
Rehabilitation has been defined as an active process by which those disabled by injury or disease can realize their optimal physical, mental and social potential with integration into the most appropriate discharge environment. Comprehensive stroke rehabilitation programs are staffed by a full range of rehabilitation professionals--nurses, physical and occupational therapists, speech-language pathologists, psychologists, social workers, recreational therapists and physicians. An interdisciplinary team skilled in the care of stroke patients provides a comprehensive rehabilitation program for each patient. Brandstater and Basmajian,1 and Roth et al.

Parkinsonian Dementia: Diagnosis, Differentiation and Principles of Treatment

Parkinsonian Dementia: Diagnosis, Differentiation and Principles of Treatment

Teaser: 

Ali Rajput, MBBS, FRCPC and Alex Rajput, MD, FRCPC
Division of Neurology, University of Saskatchewan, Saskatoon, SK.

The terms parkinsonism and Parkinson syndrome (PS) are used interchangeably. Two of the three cardinal features--bradykinesia, rigidity and tremor--are necessary to make a diagnosis of PS. Several pathological entities and neuroleptic drugs may produce PS, the most common being Parkinson's disease or idiopathic Parkinson's disease (PD), which is characterized by marked neuronal loss in the substantia nigra and Lewy body (LB) inclusions (Figure 1 is not available online). The prevalence of PS in the Canadian general population is estimated at 300 per 100,000.1 The mean age of onset is 62 years, with both incidence and prevalence rates increasing with age. In a Canadian survey of a community population over age 65 years, 3% had PS.2

Alzheimer disease (AD) is the most common dementing illness in the industrialized countries. Marked cortical neuronal loss, plaques and intraneuronal neurofibrillary tangles are pathological features of AD (Figures 2A and 2B are not available online). More than 5% of the general population over 65 years of age have AD.

Because both PD and AD occur in old age, some individuals will have both. Pathological studies suggest that this overlap is higher than expected in unselected large autopsy series.

Catechol-O-methyltransferase Inhibition in Treatment of Parkinson’s Disease

Catechol-O-methyltransferase Inhibition in Treatment of Parkinson’s Disease

Teaser: 

Zhigao Huang, MD, PhD, Clinical Fellow,
Ajit Kumar, DM, Clinical Fellow,
Joseph Tsui, MD, FRCPC, Professor, Department of Medicine, University of British Columbia, Vancouver, BC.

Introduction
Long-term treatment with dopaminomimetic drugs is often complicated by the occurrence of motor complications in Parkinson's Disease (PD) patients. This is especially true with levodopa, which remains to date the mainstay of treatment of PD. These motor complications consist of fluctuations and dyskinesias. Fluctuations refer to predictable or unpredictable changes of motor response that occur in relation to levodopa administration. Dyskinesias refer to abnormal excessive movements. Motor fluctuations can affect up to 50% of PD patients after five years of levodopa treatment.1 The main categories of fluctuations are 'wearing-off' and 'on-off.' Clinically, 'wearing-off' is characterized by a shortened duration of motor response and a rapidly waning effect in response to each oral dose of levodopa. 'On-off' refers to random fluctuations in motor response seemingly unrelated to levodopa administration.2

In early PD, the motor response to levodopa administration lasts longer than would be inferred from the plasma half-life of levodopa. Presumably, this phenomenon is related to surviving nigrostriatal neurons being able to store dopamine (DA) synthesized from exogenous levodopa, thus serving a buffer-like function.

Hallucinations in Patients with Parkinsonism: Clinical Features and Management

Hallucinations in Patients with Parkinsonism: Clinical Features and Management

Teaser: 

David J Burn, MD, MA, FRCP, Consultant & Senior Lecturer in Neurology, Regional Neurosciences Centre, Newcastle General Hospital, Westgate Road Newcastle upon Tyne, UK.

Ian G McKeith, MD, FRCPsych, Professor of Old Age Psychiatry, Department of Old Age Psychiatry, Institute for Ageing and Health Wolfson Research Centre, Newcastle General Hospital, Newcastle upon Tyne, UK.

Introduction
Parkinsonism is a common problem, particularly in the elderly. One percent of the population over the age of 65 has Parkinson's Disease (PD), rising to 2% over the age of 80. Parkinsonism is also a core feature of dementia with Lewy bodies (DLB), the second most common cause of neurodegenerative dementia, after Alzheimer disease (AD). To differentiate patients with PD who develop cognitive impairment from DLB, Consensus Criteria stipulate that parkinsonism must be present for 12 months or less for a patient with dementia to qualify for a diagnosis of DLB.1 If the extrapyramidal features are present for longer than this before the dementia develops, the diagnosis is referred to as PD with dementia.

Although parkinsonism occurs in numerous other neurodegenerative diseases, including multiple system atrophy, progressive supranuclear palsy and corticobasal degeneration, as well as AD, hallucinations are less common.

Limb Apraxia: A Clinical Perspective

Limb Apraxia: A Clinical Perspective

Teaser: 

Deborah Hebert BSc(0T), MSc(Kin) PhD candidate, Ontario Institute for Studies in Education, Clinical Educator (OT), Toronto Rehabilitation Institute Clinical Associate, Department of Occupational Therapy, University of Toronto.

Eric Roy PhD, C Psy, Professor, Departments of Kinesiology and Psychology, University of Waterloo, Graduate Department of Rehabilitation Science University of Toronto, Toronto, ON.

When a person with neurological impairment engages in an unusual action such as pouring hot water into a cup with no tea bag and stirring it with a fork, or cutting bread with a knife oriented upside down and sideways, the impairment of limb apraxia should be suspected. Apraxia has been defined as, " a neurological disorder of learned purposive movement skill that is not explained by deficits of elemental motor or sensory systems".1 While motor problems such as abnormal tone and posture, paresis, ataxia and dysmetria can coexist with limb apraxia,2,3 this movement problem is one of conceptual understanding of action and/or production of movement.4 The deficit cannot be explained by intellectual deterioration, lack of cooperation, sensory disturbances, agnosia, disrupted body schema, visuospatial disturbances or aphasia.3,5 There is evidence that aphasia and apraxia commonly co-occur, as they are predominantly found in right-handed clients with left hemisphere lesions; however, they are often clearly dissociated.

Parkinson’s Disease: An Update on Therapeutic Strategies

Parkinson’s Disease: An Update on Therapeutic Strategies

Teaser: 

Daniel S Sa, MD and Robert Chen, MBBChir, MSc, FRCPC
Division of Neurology and Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital, University Health Network, University of Toronto, Toronto, ON.

The treatment of Parkinson's Disease (PD) has undergone major changes over the past decade with the introduction of new drugs and the development of more advanced and reliable surgical procedures. However, the role of each of these different treatment alternatives is not yet clearly defined. Frequently raised questions include the most appropriate treatment in early PD and determining which patients with more advanced PD are suitable for surgery. In this review, we will attempt to address some of these issues.

Initial Treatment
The first decision to make is when to begin treatment. Since there is no therapeutic strategy proven to halt or slow disease progression, treatment initiation should be related to the level of disability. Therefore, drug therapy should be initiated when symptoms are interfering with social or occupational functions. This is usually due to impaired motor function but sometimes is related to embarrassment.

The next question is which treatment to offer. There is a long-standing debate regarding whether to start with levodopa or dopamine agonists. The levodopa proponents argue that it is still the most effective therapy for PD, and early treatment (before postural instability) has been proven to reduce mortality.

The Biological and Cognitive Effects of Estrogen on the Aging Brain

The Biological and Cognitive Effects of Estrogen on the Aging Brain

Teaser: 

Elise J. Levinoff, BSc1,2, Howard Chertkow, MD, FRCPC1,2,3
1Bloomfield Centre for Studies in Aging, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital, McGill University
2Department of Neurology and Neurosurgery, McGill University
3Division of Geriatric Medicine, Dept. of Medicine, Sir Mortimer B. Davis Jewish General Hospital, McGill University, Montreal, PQ.

Alzheimer disease (AD) is a neurodegenerative disease of elderly patients, pathologically characterized by the presence of senile plaques and neurofibrillary tangles in the brain. This pathology occurs in the cerebral cortex, specifically within the temporal lobes, resulting in impairment in cognitive domains such as short-term memory, attention, semantics, as well as aphasia and apraxia.1 Patients also show marked changes in behaviour and are impaired in activities of daily living (ADLs). The causes of AD are unknown, but age is a major risk factor. Women are at a higher risk of developing AD, although this may be due, in part, to increased longevity. Additionally, mechanisms of neuronal injury, such as the presence of cerebral infarcts and consequences of head trauma, increase the risk of developing AD. Expression of the APOE-e4 genotype has also been associated with an increase in the risk of developing AD.1

Presently, there is no cure for AD.