Changes that occur in both the visual and auditory systems with aging have been documented (Stephen et al., 2010). As noted in Chapter 51, visual acuity may decline gradually from middle age onward and may decrease rapidly in the eighth decade of life (Sjöstrand et al., 2011). Traditional testing of acuity is valid for reading but not for functional tasks such as observing walking surface variations in a darkened room. Other common changes, such as altered color discrimination and light adaptation, can translate to impaired vision and may add to any visual acuity deficit. For an individual to respond appropriately, it requires receiving an input, processing that input both perceptually and cognitively at an intellectual level or automatically at a motor level, and finally selecting the motor response that best matches the environmental requirements. An individual who wears bifocal or trifocal lenses and glances down for visually augmented feedback may see a distorted image, so inaccurate information is sent to the CNS. Thus, the motor response may be appropriate for the input being received but inappropriate for the actual environment. Conversely, an individual with visual impairment may respond adequately to environmental demands and show no signs of motor limitation. The nervous system functions on consensus and will always use other sensory systems and prior learning, if available, to determine how to respond to visual information.

As discussed in Chapter 52, hearing loss is also common among older people, the causes of which are either peripheral or central deficits generally associated with disease or biological aging (Chisolm et al., 2003). Loss of auditory acuity translates to difficulty in hearing and word recognition, or difficulty carrying on a normal conversation within a noisy environment, which may result in isolation and self-exclusion from participation in group activities. Although hearing loss itself does not impair movement, often, when the auditory portion of the eighth cranial nerve is involved, the vestibular portion is also affected (Møller, 2000). This can potentially result in vertigo and impaired balance, and increase an individual’s risk of falling (Ishiyama, 2009).

The processing of information in the cognitive and emotional areas of the CNS cannot be ignored when considering CNS changes with aging, with or without pathology. Subtle non-pathological declines do occur with aging in key cognitive domains and correlate with, but not necessarily impair, the ability to carry out daily function (Vance et al., 2010). Changes across cognitive domains and across older individuals are not uniform, with some cognitive functions demonstrating greater extents of change than others (Glisky, 2007). This underscores the need to consider the complexity of cognitive decline in clients undergoing rehabilitation. Healthcare providers must remember that when the processing or learning of cognitive materials becomes a problem, procedural learning of motor programs will become the only avenue to regain functional control over movement. Principles of motor learning then become paramount in optimizing the therapeutic environment for client improvement (Umphred et al., 2013: 69).

The healthcare provider must consider the emotional (limbic) system in all clients, especially when looking at CNS function. Emotions are controlled and modified by the limbic system. This system has extensive connections to the hypothalamus, so emotion is often expressed through regulation of the autonomic nervous system and in the tone of the striated muscle system (Groenewegen & Uylings, 2000). The hypothalamus regulates the areas of the brainstem that control the heart, lungs, internal organs and immune system.

Many behavioral syndromes have been attributed to this area of the brain. The most pertinent to older people, the ‘general adaptive syndrome’ (GAS), was described by Hans Selye in 1956 (Stojanovich, 2010; Umphred et al., 2013: 111). Today, it is considered a response to stress and can be observed in any frail individual, including older persons with fragile bodily systems. The GAS response is paradoxical to the anticipated response. Under stress, an individual generally has a sympathetic response, with an increase in heart rate and blood pressure and a fight–flight reaction. In the GAS, the same environmental conditions initially cause a sympathetic response but, over time and sometimes quickly, individuals may experience a switch to a parasympathetic reaction. Blood pressure drops, heart rate decreases, blood pools in the periphery and level of consciousness can drop. The GAS is a survival response to stress because, without such a response, the increase in heart rate and blood pressure would cause heart failure or vascular rupture. Treatment based on the GAS signs and symptoms may be aimed at increasing the sympathetic response, which may cause an even greater paradoxical reaction.

Research since 1956 has shown that hormone levels increase with stress (Lupien et al., 2009) and the amount of hormones elicited increases with age (McEwen, 2002). By virtue of advanced age, a client may be very close to multiple-system failure and would be considered frail. A client may have recently developed a disease that adds stress to an already frail system. If the corresponding treatment creates more stress in the individual, it may result in a GAS, which has the potential of evolving into a life-threatening situation. The client’s response may be to withdraw while the healthcare provider’s reaction might be to increase the level of input to motivate or heighten arousal in the client. With further withdrawal, the client can potentially die from heart failure from diminished heart rate and blood pressure. The healthcare provider should thus evaluate the client’s emotional response to the environment and try to keep a homeostatic autonomic balance. This requires being sensitive to body functions controlled by the limbic system such as respiration, blood pressure and level of alertness, as well as specific motor responses to interventions (Umphred et al., 2013: 111).

The areas typically considered to be part of the motor system are the premotor and motor areas of the frontal lobes, basal ganglia, cerebellum, brainstem, spinal cord and all the interneurons that link these systems. The thalamus plays a key role as a relay station and modulator whereas the limbic system has the ability to alter the state of motor responses both directly and indirectly (Kandel et al., 2012). The sensory areas guide and alter existing motor programs. Where the motor system begins and ends is not clear because there are so many interdependent systems that loop between one area and another. Therefore, a linear analysis is not appropriate. There is not one specific area that controls motor output, yet certain nuclear masses are responsible for specific aspects of motor function. When any one of these areas is impaired, specific clinical symptoms manifest. Motor control over base tone in striated muscles is regulated by many areas, so a deficit does not automatically reflect the involvement of a specific area. A deficit in one loop of many interconnected neuronal loops might present a clinical problem that would make it appear as if a nuclear mass or system was damaged.

Research does show that the motor system changes with age (Mora et al., 2007), although such changes cannot account entirely for the functional changes observed in older people (Mahncke et al., 2006). For example, it is accepted that there is an age differential when looking at modulation of the H-reflex which may be due to the aging neuromuscular system (Koceja & Mynark, 2000). Similarly, control over the Ia fibers as a readiness state for spontaneous movement decreases with aging (Mankovsky et al., 1982) and may be associated with a decrease in the ability to modulate inhibitory function (Fujiyama et al., 2009). Moreover, proprioceptive input has less influence on the motor cortex excitability (Degardin et al., 2011). These suggest that an aging CNS no longer has the refined regulating ability over preprogrammed synergistic patterning. Comparing performance of younger adults to older adults indicates that older people possibly begin to lose some movement automaticity and compensate through increased brain network activity (Wu & Hallett, 2005). Whether these changes are due to disuse or aging is not clear. As there are central, muscle and mechanical changes with aging, a decrease in functional ability is considered multifactorial (Degardin et al., 2011). The significance of these changes may be more meaningful following injury or disease. If the aging CNS loses some of its plasticity or ability to adapt, then it may take more time to learn new programs or alter existing ones. This might explain why aging adults seem to exhibit synergistic patterns very quickly following injury, whereas younger adults may take more time to develop the same abnormal patterns, given appropriate conditions.

A complete explanation of the specifics of the motor control system (Shumway-Cook & Woollacott, 2012) is not within the scope of this chapter, but a brief overview of the system might help the reader to understand and appreciate its complexity. The frontal lobe of the brain not only helps process the motivation to move (prefrontal) but also modulates information that travels between primary motor centers such as the basal ganglia and cerebellum (Kandel et al., 2012). In addition, it plays a primary role in regulating, but not dictating, fine and gross motor function through the corticospinal and corticobulbar systems. Normal movement results from the coordinated work of multiple areas that influence the final common pathways of motor neurons. After summating and modulating messages from other areas of the CNS, the frontal lobe sends messages concurrently to the basal ganglia and cerebellum (Kandel et al., 2012). In turn, these centers formulate new motor plans or draw upon existing plans to correctly modulate the motor system. If either a center or the loops connecting the centers is damaged or diseased, then motor function may be incoordinated and unsuited to the environmental context of the activity. The cerebellum, unlike the basal ganglia, is simultaneously aware of the peripheral kinematics through input from proprioceptors in the limbs and trunk, and from the vestibular system based on the position of the head in space. Similarly, the cerebellum is constantly updated on the existing states of the motor pool through ascending tracts that send that information directly to the anterior cerebellar lobes. Thus, the cerebellum is considered a synergistic programmer and plays a key role in feed-forward regulation of movement.

The role of the cerebellum in higher-center regulation of motor programming interfaces with the limbic system as well as the frontal lobe and basal ganglia. Deficits within the frontal lobe, limbic system or basal ganglia can affect cerebellar function and have been shown to trigger, what appears to be, cerebellar neuronal damage (Umphred et al., 2013: 601, 631–7). The cerebellum is not only responsible for helping write new programs, it also ensures that the programs being used at any one moment match the environmental context. If there is a mismatch between the desired movement sequence and environmental stimuli, the cerebellum will try to readjust the synergistic patterns and run the program that matches the environmental demands. For example, if an individual is walking on a level cement surface and suddenly the surface changes because of a crack or a hole, the cerebellum will adjust balance strategies in order to regain the center of gravity and hence allow the person to keep walking. If the perturbation created is too large, such that the cerebellum cannot correct the patterns being run, consensus of the CNS will determine what new program should be initiated.

The basal ganglia are responsible for changing the plan of movement and initiating new programs, whereas the cerebellum, in preparation for the changes to take place, regulates the state of the motor generators (base tone) and controls the force, speed and direction of movement. For example, if an individual is rising to a standing position and goes beyond vertical and starts to fall, the basal ganglia change the motor setting from rising to vertical to falling. Both the basal ganglia and cerebellum play roles in modulating posture but the specific roles are different. The basal ganglia and aspects of the cerebellum contribute in the development of new motor programs and refinement of existing ones. Both relay specific motor programming to the frontal lobes through the thalamus and down to the motor generators of the cranial and spinal neurons through the brainstem. Therefore, changes in any of these structures or in the pathways between them that occur with aging could have critical effects on normal movement. Along with pathology, such changes can become cumulative and eventually result in altered motor performance and loss of function. For example, a reported loss with age of Purkinje cells in the cerebellum has not been related to movement impairment (Rajput et al., 2011). However, this change along with cerebellar degeneration or a cerebellar stroke would be cumulative and the result might be a greater deficit than would occur in a young adult without Purkinje cell loss who develops a similar pathology.

Various studies have endeavored to describe changes in the CNS that occur with healthy aging by differentiating those with changes that mark pathological aging. Longitudinal studies have reported brain loss and multiple-domain cognitive decline over time in healthy older people, with significantly extensive changes observed on follow-up measurement in those who eventually developed mild cognitive impairment or dementia, compared to those who did not (Johnson et al., 2009). Evidence suggests that in healthy aging, brain shrinkage can be minimal and does not appear to correlate with any important limitation in functional ability. In terms of neuropathologic changes, such as the development of senile plaques or neurofibrillary tangles, even in the ‘oldest old’, or people who were at least 85 years of age, such change can be minimal and cognitive ability can remain stable (Green et al., 2000). These normal aging-related changes are in stark contrast to the severe neuronal loss found in people with neurodegenerative conditions such as Alzheimer’s disease, frontotemporal dementia and Parkinson’s disease (Yankner et al., 2008), and the extensive neuropathologic changes and steep cognitive decline seen in oldest old people with Alzheimer’s dementia (Green et al., 2000). Literature supports the concept that older people can be healthy and functionally stable into advanced age, and pathological conditions precede and determine functional loss. The aging process may affect the potential of the nervous system to adapt, but age is only one factor that influences that potential. Aging should never be considered the primary cause of functional limitations or restrictions in normal life activities.