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Parkinson’s disease

Identifying and Managing Caregiver Burden Among Spouses of Individuals with Parkinson's Disease

Identifying and Managing Caregiver Burden Among Spouses of Individuals with Parkinson's Disease

Members of the College of Family Physicians of Canada may claim MAINPRO-M2 Credits for this unaccredited educational program.

www.cfpc.ca/Mainpro_M2
Teaser: 

Kaitlyn Roland, MSc, Research Assistant, Interdisciplinary Graduate Studies, The University of British Columbia, Kelowna, BC.
Andrew M. Johnson, PhD, Associate Professor, School of Health Studies, Faculty of Health Sciences, The University of Western Ontario, London, ON.
Mary E. Jenkins, BSc(PT), BEd, MD, FRCPC, Associate Professor of Neurology, Clinical Neurological Sciences, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, ON.

Abstract
Burden is a psychological concept, a subjective interpretation by caregivers of the extent to which the caregiving experience impacts on one's health, social life, or financial status. In this article, we examine some of the predictors of caregiver burden, and look specifically at the burden experienced by caregivers of individuals with Parkinson's disease.
Keywords: Parkinson's disease, psychological health, physical health, caregiver burden

Identification and Management of Impulse Control Disorders Among Individuals with Parkinson’s Disease

Identification and Management of Impulse Control Disorders Among Individuals with Parkinson’s Disease

Members of the College of Family Physicians of Canada may claim MAINPRO-M2 Credits for this unaccredited educational program.

www.cfpc.ca/Mainpro_M2
Teaser: 


Andrew M. Johnson, PhD, Associate Professor, School of Health Studies, Faculty of Health Sciences, The University of Western Ontario,
London, ON.
H. Christopher Hyson, MD, FRCPC, Assistant Professor of Neurology, Clinical Neurological Sciences, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, ON.
Kaitlyn P. Roland, MSc, Research Assistant, Interdisciplinary Graduate Studies, The University of British Columbia Okanagan, Kelowna, BC.

Abstract
Although Parkinson’s disease is primarily considered to be a motor disorder, it has inarguable effects on cognition and personality. The cluster of neuropsychiatric sequelae known as impulse-control disorders has been of particular interest in recent years, perhaps owing to the potentially disastrous effects that such behaviors can have on individuals and families. Research has suggested that impulse control disorders are significantly more prevalent among individuals with Parkinson’s disease, particularly with regards to pathological gambling and hypersexuality, and has further suggested that these disorders are significantly and substantively affected by the use of dopamine agonists. Treatment options for impulse control disorders tend to revolve around dopamine agonist dose reduction or cessation. The use of psychosocial strategies, or deep-brain stimulation of the subthalamic nucleus may also be considered in the management of patients with impulse control disorders.
Keywords: Impulse control disorders, Parkinson’s disease, dopamine agonists service use
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An Update on the Management of Parkinson’s Disease

An Update on the Management of Parkinson’s Disease

Teaser: 

Shen-Yang Lim, MBBS, FRACP, Movement Disorder Centre, University of Toronto, Toronto Western Hospital, Toronto, ON.
Susan H. Fox, MRCP (UK), PhD, Movement Disorder Centre, University of Toronto, Toronto Western Hospital, Toronto, ON.

Parkinson’s disease (PD) is characterized by the presence of bradykinesia, rigidity, and rest tremor. Nonmotor symptoms are also very common in PD and may result in significant disability. Many approaches are available to reduce symptoms. In this article we provide an update on the management of PD. We also discuss the limitations of current treatments.
Key words: Parkinson’s disease, treatment, motor response complications, nonmotor, nondopaminergic.

Clinical Differences among Four Common Dementia Syndromes

Clinical Differences among Four Common Dementia Syndromes

Teaser: 


Weerasak Muangpaisan, MD, FRCPT, Assistant Professor, Department of Preventive and Social Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Thailand; visiting fellow, Harris Manchester College, University of Oxford, Oxford, U.K.

Cases of dementia are increasing due to longer life expectancy of the world population. Physicians should be able to recognize common dementia syndromes. After excluding reversible causes of dementia, there are four common dementia syndromes, which are Alzheimer’s disease, vascular dementia, dementia with Lewy body, and frontotemporal dementia. The key points of clinical differences of these dementia syndromes are summarized in this article.
Key words: Alzheimer’s disease, vascular dementia, dementia with Lewy body, frontotemporal dementia, Parkinson’s disease.

The Impact of Exercise Rehabilitation and Physical Activity on the Management of Parkinson’s Disease

The Impact of Exercise Rehabilitation and Physical Activity on the Management of Parkinson’s Disease

Teaser: 

A.M. Johnson, PhD, Assistant Professor, Faculty of Health Sciences, University of Western Ontario, London, ON.
Q.J. Almeida, PhD, Director, Movement Disorders Research & Rehabilitation Centre, Wilfrid Laurier University, Waterloo, ON.

Although medication therapy is generally effective in the clinical management of Parkinson’s disease (PD), additional improvement of some gross motor symptoms may be achieved through the use of nonpharmacological treatments, such as physical therapy and exercise rehabilitation. Despite the fact that PD is a neurological disorder, successful rehabilitation has been demonstrated with treatments that combine cognitive and physical approaches. While the exact mechanism through which these therapies obtain successful outcomes is still largely unknown, it is worthwhile to explore these adjunctive approaches to treating the motor output symptoms of PD.
Key words: Parkinson’s disease, movement disorders, exercise rehabilitation, physical therapy, motor control.

Nonpharmacological Management of Hypokinetic Dysarthria in Parkinson’s Disease

Nonpharmacological Management of Hypokinetic Dysarthria in Parkinson’s Disease

Teaser: 

AM Johnson, PhD, Assistant Professor, School of Communication Sciences and Disorders, the University of Western Ontario, London, ON.
SG Adams, PhD, Associate Professor, School of Communication Sciences and Disorders, the University of Western Ontario, London, ON.

In addition to its widely recognized effects on gait, posture, balance, and upper limb coordination, Parkinson’s disease (PD) can have a profound effect on speech and voice, within a cluster of speech characteristics termed hypokinetic dysarthria. Although dopaminergic therapy produces significant benefits in the early stages of PD, speech symptoms may show selective resistance to pharmaceutical therapy in patients with a disease history of more than 10 years. This article discusses the pathophysiology of PD as it relates to speech disorders and considers nonpharmaceutical therapeutic options for hypokinetic dysarthria.
Key words: Parkinson’s disease, speech pathology, dysarthria, treatment.

Pharmacological Options in Parkinson's Disease: A Treatment Guide

Pharmacological Options in Parkinson's Disease: A Treatment Guide

Teaser: 


Steven E. Lo, MD, The Neurological Institute, Columbia University Medical Center, New York, NY, USA.
Steven J. Frucht, MD, The Neurological Institute, Columbia University Medical Center, New York, NY, USA.

Parkinson’s disease (PD) is a neurodegenerative disorder that can significantly impact older patients’ quality of life. Although there are many pharmacologic options to treat PD, the clinician needs to know the indications and potential adverse effects of new medications in the older patient population. Carbidopa/levodopa remains the gold standard for treatment, and new formulations and levodopa-extenders fill specific niches. This article reviews the pros and cons of these medications in older PD patients, and demonstrates therapeutic strategies through case presentations.
Key words: Parkinson’s disease, treatment, levodopa, COMT inhibitor, aging.

Diagnosis and Management of Dementia in Parkinson’s Disease

Diagnosis and Management of Dementia in Parkinson’s Disease

Teaser: 

David F. Tang-Wai, MDCM, Department of Medicine (Neurology), University of
Toronto, University Health Network, Toronto, ON.

Keith A. Josephs, MST MD,
Department of Neurology, Mayo Clinic, Rochester, MN, USA

Neurodegenerative diseases commonly affect cortical and subcortical structures, resulting in clinical features of mixed dementia and parkinsonism. Dementia, albeit an uncommon presenting feature of Parkinson’s disease, may become a complication with disease progression. In this review we discuss the relationship of dementia and parkinsonism. We outline a clinical approach to the diagnosis and management of dementia with Lewy bodies and emphasize the importance of understanding the complexity of the disease, for which in-depth knowledge of medication side-effect profiles is a must if treatment is to be undertaken. We also briefly discuss progressive supranuclear palsy, corticobasal syndrome, and vascular dementia with parkinsonism.

Key words:
Parkinson’s disease, dementia with Lewy bodies, visual hallucinations, fluctuations, acetylcholinesterase inhibitors.

The Role of Rehabilitation in Parkinson’s Disease: A Review of the Evidence

The Role of Rehabilitation in Parkinson’s Disease: A Review of the Evidence

Teaser: 

K.H.O. Deane, BSc, PhD and C.E. Clarke, BSc, MD, FRCP, Department of Neurosciences, The University of Birmingham and City Hospital, Birmingham, UK.

Many clinicians, therapists and patients support the use of rehabilitation in the treatment of Parkinson's disease. However, systematic reviews reveal a lack of conclusive evidence to support the use of common forms of rehabilitation therapy in this movement disorder. Lack of evidence of efficacy is not proof of lack of effect. Large pragmatic randomized controlled trials are required to determine the effectiveness and safety of rehabilitation therapies for people with Parkinson's disease.
Key words: Parkinson's disease, occupational therapy, physiotherapy, speech therapy, rehabilitation.

Coenzyme Q10: New Hope for Parkinson’s Disease

Coenzyme Q10: New Hope for Parkinson’s Disease

Teaser: 

Parkinson's Disease (PD) is a progressive neurodegenerative disorder typified by bradykinesia, tremor, muscle rigidity and postural instability and is physiologically characterized by the presence of Lewy bodies and a decrease of dopaminergic neurons in the substantia nigra pars compacta. According to the Parkinson Society of Canada, approximately 100,000 Canadians currently suffer from this debilitating disorder.

Because loss of dopamine is believed to account for the impaired nerve and muscle control observed in PD, levodopa tends to be the prescribed treatment of choice. While the causes of PD have yet to be fully elucidated, a defective mitochondrial electron-transport chain appears to play a role in the pathogenesis of sporadic PD. Decreased complex I levels may expose neurons to the damaging effects of oxygen-free radicals. The inhibition of complex I via 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been demonstrated to cause human parkinsonism, thus implicating the enzyme as vital to the elucidation of the molecular causes of PD. Previous research has indicated that coenzyme Q10, the electron acceptor for complexes I and II, may be orally administered to reduce dopamine loss, thus paving the way for the potential use of Q10 as an alternative treatment for early PD.

In a multicentre, randomized, doubleblind test, Shults et al. enrolled 80 early PD patients who had not used PD medication or antioxidants for at least 60 days in order to further evaluate the role of Q10 as a mediator of functional decline in PD patients.

Within one month of selection, patients were assessed clinically and blood samples were taken to ascertain Q10 levels in plasma and complex I activity in platelets. Following a baseline evaluation session, patients were randomly assigned to a Q10 dosage of either 300, 600 or 1200mg/day or to an equivalent placebo dosage. Patients were reassessed at one, four, eight, 12 and 16 months or until sufficient disability had occurred so as to necessitate levodopa treatment. The coenzyme was administered orally four times daily in the form of a wafer that contained vitamin E to function as a lipophilic carrier. Vitamin E was also present in the placebo wafer.

Dosage reductions were not required in any of the treatment groups, demonstrating the widespread tolerability of oral coenzyme Q10 therapy. Treatment efficacy was determined using the Unified Parkinson Disease Rating Scale (UPDRS), an assessment of mental, motor and activities of daily living (ADL) skills. The adjusted mean UPDRS changes were +8.81 for the 300mg/d group, +10.82 for the 600mg/d group, +6.69 for the 1200mg/d group and +11.99 in the placebo group. The primary analysis, a test for correlation between dosage and the mean change in UPDRS score, determined a p value of .09, signifying a linear trend according to prespecified criteria. The greatest reduction in UPDRS score was seen in the 1200mg/d group in the ADL realm of the UPDRS.

Mean plasma Q10 levels were significantly increased in all test groups. Mitochondrial assays demonstrated that complex I activity, which proceeds independently of endogenous coenzyme Q10, was unaffected in the various treatment groups. Conversely, the NADH to cytochrome-c reductase, which depends largely on endogenous Q10 levels, showed increased activity with increased Q10 dosage.

The findings of this clinical trial propose a role for orally administered Q10 in mitochondrial function. However, this role remains questionable with regards to PD, given that the results found in plasma have yet to be replicated in the brain. The authors suggest that high dosages of Q10 may be used in the treatment of neurological diseases which are characterized by defective complex I or complex II enzymes, such as PD and Huntington disease. The linear correlation between dose and decreased cognitive decline suggests that the effect of even higher Q10 dosages should be explored. Additionally, due to the complex interaction between genetic defects and environmental insult which likely contributes to PD, further investigation into the precise mechanism of dopamine loss is imperative for future PD alleviation.

Source

  1. Shults CW, Oakes D, Kieburtz K, et al. Effects of coenzyme Q10 in early Parkinson Disease. Arch Neurol 2002;59:1541-50.