Part 1: Introduction, Head and Neck, and Cranial Nerves

David J. Gladstone, BSc, MD, Fellow, Cognitive Neurology and Stroke Research Unit, Sunnybrook and Women's College Health Sciences Centre and Division of Neurology, University of Toronto, Toronto, ON.

Sandra E. Black, MD, FRCPC, Professor of Medicine (Neurology), University of Toronto; Head, Division of Neurology and Director, Cognitive Neurology Unit, Sunnybrook and Women's College Health Sciences Centre, Toronto, ON.

Abstract
This four-part series of articles provides an overview of the neurological examination of the elderly patient, particularly as it applies to patients with cognitive impairment, dementia or cerebrovascular disease. The focus is on the method and interpretation of the bedside physical examination; the mental state and cognitive examinations are not covered in this review. Part 1 begins with an approach to the neurological examination in normal aging and in disease, and reviews components of the general physical, head and neck, neurovascular and cranial nerve examinations relevant to aging and dementia. Part 2 covers the motor examination with an emphasis on upper motor neuron signs and movement disorders. Part 3 reviews the assessment of coordination, balance and gait. Part 4 discusses the muscle stretch reflexes, pathological and primitive reflexes, sensory examination and concluding remarks.

Roland R. Tremblay, DSc, MD, PhD, Professor Emeritus of Medicine, Laval University, Quebec City, QC.

Introduction
In both sexes, aging is associated with a progressive reduction in skeletal muscle mass and strength, although this may be masked by increases in subcutaneous fat or abdominal obesity that give the impression of stable body weight. Progressive frailty, however, occurs on a more global level with seniors "affected by multiple chronic diseases which cause physical and functional limitations."¹ These comorbid diseases may cause a systemic stress, which by itself (excess cortisol secretion), or by virtue of its suppressive action on the pituitary-gonadal axis, leads to a decline in androgen production. While the tendency to associate andropause and androgens has become increasingly common, the causal link between male hormone deficiency and the clinical disorder andropause still remains a weak one. A medical anthropologist is certainly likely to qualify the association as a reductionist vision of the frailty syndrome. In a sense, this vision serves the interests of both patients and physicians: it facilitates the diagnostic approach and the treatment strategies in an aged population, estimated at 20%, that seeks medical attention because of frailty, low mental and physical energy, depression-like symptoms and sexual hypofunction.

Peter J. Pommerville, BA, MD, FRCS(C), Consultant Urologist, Vancouver Island Health Authority, Victoria, BC; Principal Investigator, Can-Med Clinical Research Inc., Victoria, BC.

Introduction
Erectile Dysfunction is a significant and common medical problem. The National Institutes of Health has defined erectile dysfunction as "the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual performance."¹ The nature of sexual dysfunction is more precisely defined by the term erectile dysfunction (ED) than by the term impotence.¹

ED is a clearly defined problem that the medical practitioner must differentiate from premature ejaculation, orgasmic dysfunction and Peyronie's disease.

Prevalence of Erectile Dysfunction
According to the NIH Consensus Development Panel, ED may affect as many as 30 million males in the U.S.¹ Data collected by Statistics Canada indicate that as many as three million Canadian men may suffer from ED. However, it is estimated that fewer than 20% seek treatment.²

Epidemiological studies conducted in the U.S. provide the most extensive information on the prevalence of ED. One such study that is often referred to is the Massachusetts Male Aging Study (MMAS).³ This study demonstrated a combined prevalence of minimal, moderate and severe ED in 52% of non-institutionalized men aged 40 to 70 (Figure 1). Of these, 10% reported complete ED, 25% reported moderate ED and 17% minimal ED.

Stephen Holzapfel, MD, CCFP, FCFP, Medical Director, Sexual Medicine Counselling Unit,
Sunnybrook and Women's College Health Sciences Centre;
Associate Professor, Department of Family and Community Medicine,
University of Toronto, Toronto, ON.

Sexual function and self-perception is integral to our sense of self and well-being. Yet we live in a society that desexualizes older people, especially women. Aging women experience changes in their sexuality that are often associated with negative effects on mood. Can we help women who are distressed by these changes?

Mood and Sexuality Changes Associated with Menopause
Most women make the transition through menopause with few long-term negative effects on their sexuality. Two-thirds of women in relationships are still sexually active in their 60s, with a gradual decline to about 25% of couples in their 80s. While many are comfortable with these changes, some are distressed by the loss of physical intimacy. The absence of a partner due to death, divorce or partner illness curtails women's sexual lives more often than do their own medical issues. Aging men face increasing erectile dysfunction, with one in seven men experiencing complete impotence by age 70.¹ Given that North American women marry men who are on average four years older than themselves, and that men die six years sooner, most women face up to a decade of widowhood.

Laumann et al.

Shawna L. Johnston, MD, FRCSC, Assistant Professor, Department of Obstetrics and Gynecology, Queen's University, Kingston, ON.

Abstract
The population of postmenopausal women in Canada is growing rapidly. It is now estimated that there are more than four million women in Canada over the age of 50. Menopause, hormone replacement and the sequelae of estrogen deprivation will become important foci for health care in this century.

Urogenital aging occurs as a result of estrogen deprivation in menopause and of tissue aging itself. Problems originate from the lower urinary tract (urethra and bladder) and from the vagina. Vaginal complaints include dryness, dyspareunia, discharge and/or bleeding. Estimates of prevalence suggest that 40-50% of postmenopausal women are affected. These symptoms, while not life-threatening, can be extremely uncomfortable and limiting, and can negatively impact on quality of life.

Estrogen replacement therapy has long been the mainstay of treatment for vaginal atrophy. Both oral and vaginal estrogen are effective, though the vaginal route is often chosen because it avoids the enterohepatic circulation and can therefore be given in much lower doses. Estrogen can be administered vaginally as a cream. Newer methods of delivery include estradiol vaginal tablets and sustained release intravaginal estradiol rings. Effective nonhormonal alternatives include the vaginal moisturizer, polycarbophil.

Nutrition is a key factor in successful aging. Eating well can help older adults maintain their health and independence. A healthy, well-nourished senior is more likely to feel good, stay well and be able to contribute as a vital member of their family and community.

Many seniors are interested in healthy eating and will make significant changes in their food choices in an effort to maintain and improve their health.¹ Dietitians offer the following sound advice to older adults motivated to stay well by eating well:

• Emphasize whole or enriched grain products such as bran cereals, multigrain bread, barley and brown rice;
• Drink plenty of fluids to assist digestion and prevent dehydration;
• Add colourful fruits and vegetables to stimulate appetite and provide essential vitamins and minerals;
• Help strengthen bones by improving intake of calcium and Vitamin D. Choices include milk, yogurt and cheese;
• For high-quality protein, include foods such as beef, poultry, fish, eggs, tofu and legumes;
• Choose lower fat foods more often, add less fat in cooking and at the table;
• Eat and drink enough to maintain a healthy weight.

Most importantly, seniors are encouraged to stay active and make healthy eating a pleasurable part of their daily lives.

For many older adults, physiological, functional and environmental realities of aging interfere with healthy eating.

Ahmed Al-Badr, MBBS, FRCSC, Clinical Fellow
Harold P. Drutz, MD, FRCSC, Professor and Head of Division, Division of Urogynecology and Pelvic Reconstructive Surgery, Department of Obstetrics and Gynecology, University of Toronto, Mount Sinai Hospital, Toronto, ON.

Pelvic organ prolapse (POP) refers to protrusion of the pelvic organs into, or out of, the vaginal canal. It is the result of damage, both direct and indirect, to the vagina and its pelvic support system. Direct injuries include detachments and lacerations of the connective tissue support system or stretching and tearing of the levator ani muscles, most commonly as a result of vaginal delivery. Indirect injury includes hypoestrogenic atrophy and denervation. POP may involve the urethra, bladder, uterus, intestine and rectum.¹ (Figure 1).

Normal Pelvic Support System in Females
It is primarily the pelvic diaphragm, the endopelvic fascia and the vagina that provide support for the pelvic organs (Figures 1 and 2). The pelvic diaphragm is made up of a bilateral paired group of striated, posteriorly fused levator ani muscles and its coverings. The urethra, vagina and the rectum pass through an anterior separation between the levator ani, called the levator hiatus, as they exit the pelvis (Figures 3 and 4).

Cynthia M. Westerhout, MSc^1,2 and Eric Boersma, PhD¹
From the ¹Department of Cardiology, Erasmus Medical Centre, Rotterdam, The Netherlands and the ²University of Alberta, Edmonton, AB.

Introduction
The chain of events leading to acute coronary syndromes (ACS), including unstable angina (UA) and non-ST-segment elevation (NSTE) or ST-segment elevation myocardial infarction (STEMI), is triggered by the disruption of an atherosclerotic plaque, which leads to the formation of a platelet-rich thrombus within a coronary artery.^1,2 The inhibition of platelet aggregation is fundamental to the treatment of these patients; however, standard antiplatelet agents such as aspirin do not completely obstruct this activity. Advances in understanding the pathophysiology of ACS have to the recognition of the activation of the glycoprotein IIb/IIIa (Gp IIb/IIIa) receptors on platelets as the final common pathway leading to platelet aggregation. With this target in mind, pharmacological treatment of ACS has been propelled into a new era with agents that completely inhibit platelet aggregation.

Serge Gauthier, MD, FRCPC, Neurologist, McGill Centre for Studies in Aging, McGill University, Montreal, QC.

Introduction
The advent of cholinesterase inhibitors (CI) as regular prescription drugs for the treatment of Alzheimer disease (AD) in mild to moderate stages has created opportunities for a proactive role among primary care practitioners with interest in a geriatric practice. The Canadian Consensus Conference on Dementia original report,¹ and its update,² clearly support the role of primary care physicians in the diagnosis and treatment of AD. A new challenge is the assessment of response to CI in individual patients. This review will examine the evolving expectations of response to treatment since 1986, when tacrine was first described as an effective drug,³ and will conclude with current realistic goals at therapeutic doses of donepezil, rivastigmine and galantamine--improvement in apathy peaking after three months of therapy and one year of stability for cognitive, functional and behavioural symptoms, followed by a decline parallel to natural history.⁴

Responders in Randomized Clinical Studies
The early descriptions of the response to CIs such as tacrine, included 'return to playing golf,'³ which set treatment expectations to a return to previous complex activities. A Canadian double-blind multicentre study did not find such dramatic effects.

Chris MacKnight, MD, MSc, FRCPC, Division of Geriatric Medicine, Dalhousie University, Halifax, NS.

Introduction
Vascular dementia is common, and currently there is no accepted therapy aimed at the cognitive symptoms. Prevention of further strokes is, of course, well established.¹ Evidence is accumulating that the cholinesterase inhibitors, proven therapy in Alzheimer disease (AD), may also be of use in vascular dementia (VaD). This paper will summarize that evidence.

Epidemiology of Vascular Dementia
Vascular dementia can be diagnosed when there is a high degree of suspicion that cognitive impairment and stroke are related. Various criteria exist, which unfortunately do not overlap to any great extent, but all share several features.² These include: the presence of stroke, either clinical or found on neuroimaging; the presence of focal neurologic signs, such as asymmetric power or a positive Babinski response; and a characteristic course, with a sudden onset or stepwise progression. For the highest degree of confidence in the diagnosis, a temporal relationship between the stroke and the dementia is required.

In most surveys of older adults, vascular dementia is the second most common cause of dementia in the community, after AD. In Canada, the prevalence of VaD is 1.5% in people 65 and over, and 5.1% for AD.³ Other surveys have found similar values.