James E. Galvin
Neurologic Signs in Older Adults
Neurologic disorders are a common cause of morbidity, mortality, institutionalization, and increased health care costs in the older adult population.1 Not only does advancing age increase the frequency and severity of neurologic disease, but it may also play an important role in modifying disease presentation. Although physical difficulties can occur independently of cognitive decline, physical difficulties coexist with cognitive impairment in many seniors.2 Data from the Behavioral Risk Factor Surveillance System have suggested that cognitive impairment is present in 12.7% of individuals aged 60 years and older.3 Of these, 35.2% also report physical functional difficulties. Having cognitive and physical functional impairment may be particularly taxing on the affected individuals and their caregivers. Thus, the geriatric neurologic examination is a critical part of any encounter with older adults but can be challenging, even for the most experienced clinicians. Normal aging may be associated with the loss of normal neurologic signs or the exaggeration of others. It may be associated with the appearance of findings considered abnormal in younger patients or the reappearance of physical signs usually seen in infancy and early stages of development.
The geriatric neurologic examination is also frequently influenced by the involvement of other systems (e.g., endocrinologic or rheumatologic disease), the co-occurrence of multiple chronic conditions in a single patient, and the presentation of non-neurologic disorders (e.g., myocardial infarction, urinary tract infection, fecal impaction) as neurologic signs ( e.g., gait difficulty, confusion). When establishing a neurologic diagnosis, the clinical history—history of the present illness, past medical history, social habits, occupational experience, family history, and review of systems and medications—assists the clinician in generating a differential diagnosis that can be further explored and refined by pertinent observations documented on the mental status and neurologic examinations. Therefore, it is important to appreciate the multitude of age-related changes in the central and peripheral nervous systems (Box 18-1).
Mental Status
Because the frequency of cognitive disorders increases dramatically with advancing age, examination of mental status is one of the most important components of the neurologic examination. Unfortunately, it is often one of the more time-consuming parts of the examination and can be difficult to interpret, particularly in new patients for whom no baseline performance data exist. In general, the fund of knowledge and vocabulary continues to expand throughout life, and learning ability does not appreciably decline in older adults without a neurocognitive disorder. Cognitive changes associated with normal aging include decreases in processing speed, cognitive flexibility, visuospatial perception (often in conjunction with decreased visual acuity), working memory, and sustained attention.4 Other cognitive abilities such as access to remotely learned information and retention of encoded new information appear to be spared in aging, allowing their use as sensitive indicators for disease processes.3
Crystallized intelligence characterized by practical problem solving, knowledge gained from experience, and vocabulary tends to be cumulative and does not generally decline with aging.5 On the other hand, fluid intelligence characterized by the ability to acquire and use new information, as measured by solutions to abstract problems and speeded performance (e.g., performance on the Raven’s Progressive Matrices and Digit Symbol of the Wechsler Adult Intelligence Scale) has been shown to decline gradually with aging.6
Longitudinal studies of memory and aging demonstrate considerable variability of cognitive abilities between different individuals (interindividual variability) as well as of different cognitive domains within the same individual (intraindividual variability).7 At least part of this variability may be attributed to different study designs; however, it is very important to take the intraindividual and interindividual variability into consideration when defining neuropsychological norms for older adults to ensure that clinical samples are not contaminated by individuals with mild forms of cognitive impairment. Some authors have suggested that age-weighted rather than age-corrected norms for cognition should be used, whereas other investigators have stressed the influence of other factors such as culture, experience, educational background, and motor speed on cognitive performance. For example, whereas older adults generally perform less well on the verbal and performance subtests of the Wechsler Adult Intelligence Scale compared with young adults, these differences are minimized when corrected for motor slowing and educational level. Other situational factors that may affect individual performance on cognitive tasks include fatigue, emotional status, medications, and stress. Moreover, it may be very difficult to attribute impaired cognition to aging in the presence of underlying conditions such as depression, dementia, and delirium, all of which are common, and often unrecognized, in the older adult population.8
The elements of a comprehensive mental status examination include the assessment of cognitive, functional, and behavioral domains. The initial contact with the patient affords the opportunity to assess whether a cognitive, attention, affective, or language disorder is present. If available, questioning of an informant may reveal changes in cognition, function, and behavior of which the patient is not aware or denies.
Screening for cognitive disorders in the older adult may include performance and informant measures. Examples of brief tests of mental status include the Mini-Mental State Examination,9 Mini-Cog,10 and Montreal Cognitive Assessment.11 Decrements in cognitive ability are compared to published norms, often adjusted for age and education. Examples of brief informant assessments include the AD812 and Informant Questionnaire on Cognitive Decline in the Elderly.13 These scales detect intraindividual decline by comparing current performance on cognitive and functional tasks to prior levels of performance, although patients may perform differently, depending on the level of impairment.14 Combining performance and informant measures may increase the likelihood of detecting cognitive disorders.15
Cranial Nerve Function
Smell and Taste
Normal aging is associated with decrements in olfaction at threshold and suprathreshold concentrations. Older adults also have a reduced capacity to discriminate the degree of differences between odors of different qualities and have impaired performance on tasks that require odor identification.16 Impaired olfaction with aging may be due to structural and functional changes in the upper airway, olfactory epithelium, olfactory bulb, or olfactory nerves.17 It is important to recognize that although impaired smell can be associated with aging, it can also be the result of medications, viral infections, and head trauma. Moreover, there appears to be early involvement of olfactory pathways in neurodegenerative diseases such as Alzheimer disease (neurofibrillary tangles)18 and Parkinson disease (Lewy bodies).19 Taste, which in turn is greatly dependent on olfaction, also decreases with advanced age, with a reduced sensitivity for a broad range of tastes compared to young adults.20,21 Although the number of taste buds does not seem to be significantly decreased in older adults, some studies have suggested decreased responses in electrophysiologic recordings from taste buds. A number of other factors, such as medications, smoking, alcohol, head injuries, and dentures, may contribute to decreased taste and smell.
Vision
Age-related changes have been documented in visual acuity, visual fields, depth perception, contrast sensitivity, motion perception, and perception of self-motion in relation to external space (optical flow). Visual acuity declines due to a number of ophthalmologic (e.g., cataracts, glaucoma) and neurologic (e.g., macular degeneration) causes. Pupillary size is typically smaller with age, and pupils are less reactive to light and accommodation, forcing many older adults to use glasses for reading.4 There is also a restriction in eye movement in upward gaze. Anatomic and physiologic studies have demonstrated a gradual decline in photoreceptors after the age of 20 years, resulting in decreased visual acuity in older adults.22,23 This is especially apparent in conditions with low contrast and luminance. There is also age-related impairment in accommodation, which leads to farsightedness (presbyopia) and a decrease in accommodation due to rigidity of the lens.24 Relaxation and accommodation times increase progressively and peak around the age of 50 years. Therefore, many older adults are forced to use glasses for reading. Moreover, ophthalmologic conditions such as cataracts, glaucoma, and macular degeneration occur commonly with advancing age and contribute significantly to the decreased visual acuity seen with aging.
Pupillary abnormalities can also been seen with normal aging. These include smaller pupils (senile miosis), which may be due to decreased preganglionic sympathetic tone, sluggish reaction to light, and decrease or even loss of the near or accommodation response.
Age-associated changes in extraocular motility include decreased velocity of saccades, prolonged latency, decreased accuracy, and prolonged duration and reaction time.25 There is also an age-related limitation of upgaze, but not downgaze, slowing of smooth pursuits. and impaired visual tracking.26 Vertical gaze changes begin in middle age and decline in the upward plane from 40 degrees between the ages of 5 and 14 years to 16 degrees between the ages of 75 and 84 years.27,28 Vertical gaze palsy is an important consideration in the evaluation of driving abilities in older adults (street signs, traffic lights). Other changes of eye movements with aging include loss of the Bell phenomenon—upward and outward deviation of the eyes in response to attempted forced closure of the eyelids.
Hearing and Vestibular Function
Gradual loss of cochlear hair cells, atrophy of the stria vascularis, and thickening of the basement membrane may account for the impaired hearing commonly seen with aging. This is often referred to as presbycusis and predominantly affects higher frequencies.29,30 Other changes include impaired speech discrimination, increase in pure tone threshold averages (approximately 2 dB/year), and decreased discrimination scores.31 Vestibular function may also be affected with age.32 There is a decrease in vestibulospinal reflexes and in the ability to detect head position and motion in space. These may be secondary to loss of hair cells and nerve fibers, as well as neuronal loss in the medial, lateral, and inferior vestibular nucleus in the brainstem.26
Motor Function
There is a progressive decline in muscle bulk associated with aging, sometimes referred to as sarcopenia. This is most obvious in the intrinsic muscles in the hands and feet, particularly the dorsal interossei and thenar muscles, as well as around the shoulder cap (deltoid and rotator cuff muscles).4 Atrophy of the thenar muscles, without weakness or fasciculations, may be present in over 50% of older adult patients.33 Results of different longitudinal studies have been inconsistent regarding the predominant fiber type affected by aging, with reports of loss of type IIb (fast twitch) fibers, reduction in the percentage of type 1 fibers, with no change in type I or II mean fiber area, decrease in the capillary-to-fiber ratio, and increase in the percentage of type I fibers.34 The decrease in muscle mass is associated with electrophysiologic evidence of denervation and muscle fiber atrophy.35 However, the consistent presence of fasciculations is not a normal sign of aging and, if present, should warrant a search for pathologic causes (e.g., motor neuron disease, compressive cervical myelopathy, multifocal motor neuropathy). A decrease in muscle strength often accompanies the decrease in muscle bulk,36 with up to a 50% decrease in maximal voluntary contraction force and twitch tension in the quadriceps. Hand grip strength decreases significantly after the age of 50 years, but strength in the arms and shoulders does not change until after the age of 60. Weakening of abdominal muscles may accentuate lumbar lordosis and contribute to low back pain.4
In addition to motor bulk and strength, there also appears to be loss of speed and coordination of movement with aging.37 Speed of hand and foot tapping was reduced by 20% in one study, and a mild terminal tremor, mild bradykinesia, rigidity, and mild dysmetria on finger-nose and heel-shin testing can also be found in isolation in up to 40% of older adults. In one study of 467 patients, the prevalence of parkinsonian signs defined as the presence of signs of two or more categories (rigidity, bradykinesia, tremor, gait disturbance) increased gradually from 14.9% for those aged 65 to 74 years to 52.4% for those 85 years and older.38 These may interfere with activities of daily living, such as dressing, eating, and getting out of a chair, and may be an important source of disability. Another finding in that study was that the presence of parkinsonism was associated with a twofold increase in mortality, mostly due to gait instability.
Paratonia
Paratonia (gegenhalten) represents increased motor tone with rapid passive movements of the limbs (flexion and extension), often suggestive of deliberate resistance.39 Unlike the rigidity of Parkinson disease, it is not constant and tends to disappear with slow movements of the limbs. Paratonia can be detected when the patient’s arms, suspended 15 cm above the lap, remain elevated after being released, despite instructions to the patient to relax. The prevalence of paratonia increases with advancing age, with a prevalence of 4% to 21%.4 It is considered by some to be a postural reflex or a cortical release sign. Similar to other primitive release signs, its prevalence is higher in patients with Alzheimer disease and other forms of dementia and correlates with the severity of cognitive impairment. Paratonia may also represent a sign of age-related changes in the basal ganglia.
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