1. OVERVIEW AND DESCRIPTION
Understanding of the neurologic consequences of healthy aging is important to Physical Medicine & Rehabilitation for a number of reasons. First, many physiatrists treat older adults in their practices. Second, distinguishing neurologic changes of healthy aging from those of age-related disease influences decisions about the need for evaluation and treatment. Third, as the population ages, PM&R physicians will see increasing numbers of healthy older adults who desire recommendations for physical activities they can participate in for health maintenance and disease prevention. Physiatrists are uniquely qualified to provide such guidance, which takes into account the unique characteristics of the healthy older adult.
Information from human research is presented in this article. However, some information is only available from animal research, due to the difficulty of performing invasive anatomical and physiological studies in humans.
Prior to presenting details, several introductory remarks are in order regarding normal biological aging.
1) For the purposes of this section, biological aging is defined as a process of progressive, intrinsic, and cumulative cellular and organ changes that result in decrease of the organism’s ability to withstand stressors. These changes eventually result in the organism’s decreased ability to survive. Biological aging is also characterized by universality across populations, cultures, and physical environments.1
2) The exact causes of aging remain unknown. Many theories of aging are supported by experimental evidence, but a single unifying framework has yet to be found. Prominent themes in these theories include accumulation of free radical damage, imbalance between cellular damage vs. repair, and disorders of mitochondrial function.2
3) A well-known characteristic of biological aging is increased variability in the normal presentation, whether it be in populations, organ systems, or tissues.3 Not all cells in a tissue age at the same rate, nor do all tissues and organs age at the same rate within an organism. Likewise, in populations of healthy older adults, there is a wide range of what can be considered to be normal function.4,5 This variability at times can blur the distinction between healthy aging and disease of aging. Therefore, the clinician may benefit from observation of patients over time, in order to better determine the nature and rate of change in the neurologic findings.3
2. RELEVANCE TO CLINICAL PRACTICE
In this section, the framework of a standard neurologic examination will be used to briefly summarize common neurologic changes of healthy aging. By definition, these changes are not sufficient to impair an individual’s ability to function well, commensurate with their age. They are not subclinical presentations of diseases of aging. As noted above, the considerable variability in aging populations will result in a wide range of presentations within these categories.
Mental status, cognition4-9
The most consistently found change in cognition of healthy older adults is slowed processing speed, especially for new or complex information. Indeed, some experts have stated that, if processing speed is accounted for, there may not be many other significant changes in other aspects of cognition in aging.9 Other common changes of cognitive aging include: decreased mental flexibility, decreased maintenance of sustained and/or divided attention, and decrements in working memory (ability to manipulate information held in short term memory/fluid intelligence). Not decreased, however, are semantic memory (vocabulary, recall of facts learned in past/crystallized intelligence), and ability to learn new skills. Aging changes in other sensory systems can influence testing performance, and so need to be accounted for.
The anatomic findings associated with these cognitive changes are not uniform throughout the brain. Findings from human MRI studies include decreased volume of gray matter in the prefrontal cortex (associated with executive functioning) and in the hippocampus (associated with memory). This decrease is not thought to be due to large amounts of neuron loss, but rather to decrease in neuron soma size, decrease in synapse number and decrease in complexity of dendrite branching. MRI studies of older brains have also reported decrease in white matter volume. This finding is related to increased myelin degeneration, decreased myelin repair, and shortening of myelinated nerve fibers. These changes in myelination are associated with slowed nerve conduction velocities. Due to the volume loss of cortex and white matter, ventricles may enlarge slightly. Accumulation of neurofibrillary tangles and “senile” plaques also occurs in brains of healthy older persons. Physiological studies have shown that older adults activate bilateral prefrontal cortex regions during specific cognitive tasks, as compared to unilateral activation in younger adults. This pattern may represent compensation for aging-related cognitive functions, but more research needs to be done to verify this hypothesis.
Depression is not considered a requisite neurological change of aging. However, with the potential multiple stresses that older adults may experience (retirement, death of spouse, loss of physical health, etc.), depression is an important condition to recognize and treat. The incidence and prevalence of depression in the geriatric age group is projected to increase as the world’s population ages.10 Theories regarding the etiology of depression include decrease in neurotransmitter function and alterations in cell signaling,11 factors that are also influenced by aging.9
Cranial Nerves 4,5
Age-related stiffening of the lens results in decreased lens accommodation for near vision (presbyopia). Other vision changes of aging include: slowed adjustment to low light, decreased color discrimination, decreased depth perception, and decreased ability to detect contrast. Visual acuity may also decrease, and upward gaze can be limited. Many of these visual changes are related to a drop-out of photoreceptors and retinal ganglion cells. Slowed adjustment to dark is also related to slowed pupillary reflexes, and color discrimination is affected by yellowing of the lens with aging.
Hearing 4,5,13, 14
High frequency hearing loss (presbycusis) becomes more common with increasing age. This problem is often related to atrophy of the capillary bed in the stria vascularis, or damage to cochlear hair cells, but can also be significantly influenced by environmental noise exposure. High frequency hearing loss can affect ability to discern specific speech sounds, such as consonants. Older adults may also have difficulty understanding speech in noisy environments. This problem is thought to be due not only to hearing loss, but also to altered auditory processing. The increased cognitive effort of listening may cause the older adult with hearing loss to show decreased memory for spoken information.
Motor system (strength, tone, posture and gait) 4,5,15,16
Sarcopenia is the age-associated loss of muscle mass and function, which results in decreased muscle strength and power. Sarcopenia is also associated with increased motor unit size due to loss of large, fast-conducting motor neurons in the spinal cord. Collateral innervation often occurs by slower-conducting, smaller motor neurons. Animal studies have also identified age-related alterations in neuromuscular junction structure, including increased branching of the pre-synaptic nerves, and receptor redistribution in the post-synaptic membrane.
There are several aging-related changes in posture and movement. Posture may become mildly forward flexed, gait speed may be slowed, and arm swing decreased. Step length shortens and duration of double support phase increases. These changes may be influenced also by the presence of age related-diseases such as osteoarthritis. Taken together, such changes can predispose the older adult to the serious problem of falls.
Deep tendon reflexes at the ankles may be decreased or absent in ~5-10% of older adults. Other deep tendon reflexes are usually preserved. So-called pathological reflexes (palmo-mental, glabellar, snout, etc.) may be present in the healthy older adult for unknown reasons. Observation of the patient over time could be helpful in determining whether or not they may indicate sub-clinical neurologic disease.
The most common sensory change in older adults is a decrease in lower extremity vibratory sensation (~50% if over age 75 yrs.). Upper extremities tend not to show this decrement. Sensation for light touch and pain are generally preserved.
Due to the enlargement of motor units with aging, there can be a decline in accuracy of fine motor task performance. Healthy aging is not associated with ataxia.
Older adults experience shorter sleep cycles, more frequent night-time waking, and earlier morning waking.
Aging motor and sensory peripheral nerves show myelin degeneration/regeneration, and decreased axon diameter. These changes result in slowed nerve conduction velocities, and decreased action potential amplitudes. Due to anterior horn cell loss, with reinnervation, aging motor unit action potentials (MUAPs) have longer durations, more phases, and lower amplitudes than in younger adults.
Pertinence to patient care:
Care of older adults may be enhanced by implementing the following suggestions:
a) Cognition and communication: allow adequate time for information processing and learning, use less complex sentence structure, present one task at a time
b) Depression: consider exercise an important part of the prevention and treatment of depression. Aerobic and strength training have both been shown to improve mood.10
c) Vision: provide adequate lighting without glare, identify potential environmental hazards (i.e. stairs) with high-contrast visual cues.18
d) Hearing: provide quiet environments for conversation, present spoken information slowly and clearly, position listeners so they can see the speaker’s face and lips, and encourage hearing aid use as appropriate. However, hearing aids will not assist with auditory processing, given its relationship to aging changes in the central nervous system.
e) Sarcopenia: include resistance training in exercise recommendations
f) Falls risk, posture and gait changes: include exercise in the prevention or treatment plan. Options include specific balance exercises, aerobic and resistance training. tai chi and/or function-based exercises.19
Additionally, in order to evaluate and follow an older adult’s motor function and balance, a number of standardized assessment tools are available for use in the clinic. Such tools include the 6 Minute Walk Test, the Timed Up and Go test, and the Berg Balance Assessment (Rehabmeasures.org).
g) Sleep: recognize the influence that inadequate sleep can have on cognitive function.
3. CUTTING EDGE/UNIQUE CONCEPTS/EMERGING ISSUES
The extreme complexity of the nervous system leaves much that is yet to be studied. New technology (functional MRI, positron emission tomography, etc.) enables non-invasive and quantitative study of anatomic and physiological parameters in human brains that were not accessible in the past. Use of such techniques may not only provide additional knowledge about normal neurologic function, but could also potentially provide data to allow for earlier diagnosis of neurologic disease, thereby assisting in the provision of early improved therapies.
4. GAPS IN KNOWLEDGE/EVIDENCE BASE
The relationship between exercise, physical fitness, and cognition is a new and growing area of study. Quantitative MRI techniques have documented increased gray matter volumes in prefrontal cortex and hippocampus in individuals who are at least moderately physically active. 20 However, the relationships between cortical volume and cognitive function are just beginning to be understood. Much more research is necessary before firm conclusions can be reached about the contribution of exercise to cognitive health in aging.
- Ljubuncic P, Reznick A. The evolutionary theories of aging revisited-a mini-review. Gerontology. 2009; 55:205-216).
- Weinert BT, Timiras PS. Physiology of aging, Invited Review: Theories of aging. J Appl 2003;95:1706-1716.
- DiGiovanna AG. Human Aging, biological perspectives. 2nd ed. Boston, MA: McGraw Hill Higher Education; 2000:16.
- Drachman DA, Swearer JM. Neurological evaluation of the elderly patient. In: Albert ML, Knoefel JE, Eds. Clinical Neurology of Aging. 3rd ed. New York, NY: Oxford University Press; 2011: 41-54.
- Larner AJ. Neurological signs of ageing. In: Sinclair AJ, Morley JE, Vellas B, Eds. Pathy’s principles and practice of geriatric medicine. 5th ed. West Sussex UK: Wiley-Blackwell; 2012:609-616.
- Bartzokis G, Lu PH. Brain volume: Age-related changes. In: Hof PR, Mobbs CV, Eds. Handbook of the neuroscience of aging. Burlington, MA: Academic Press Elsevier; 2009:27-38.
- Kensinger EA. Cognition in aging and age-related disease. In: Hof PR, Mobbs CV, Eds. Handbook of the neuroscience of aging. Burlington, MA: Academic Press Elsevier; 2009:249-256.
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- Scheibel AB. Aging of the brain. In: Hof PR, Mobbs CV, Eds. Handbook of the neuroscience of aging. Burlington, MA: Academic Press Elsevier; 2009:5-10.
- Eyre H, Baune B, Lavretsky H. Clinical advances in geriatric psychiatry. A focus on prevention of mood and cognitive disorders. Psychiatr Clin N Am. 2015: 495-514.
- Sadock BJ & Sadock VA. Kaplan & Sadock’s Concise Textbook of Clinical Psychiatry. 3rd ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2008: 200-205.
- Blanks JC, Dorey CK. Sensory aging: vision. In: Hof PR, Mobbs CV, Eds. Handbook of the neuroscience of aging. Burlington, MA: Academic Press Elsevier; 2009:199-214.
- Pichora-Fuller MK, MacDonald E. Sensory aging: hearing. In: Hof PR, Mobbs CV, Eds. Handbook of the neuroscience of aging. Burlington, MA: Academic Press Elsevier; 2009:193-198.
- Stine-Morrow EAL, Shake MC. Language in aged persons. In: Hof PR, Mobbs CV, Eds. Handbook of the neuroscience of aging. Burlington, MA: Academic Press Elsevier; 2009:287-292.
- Aagaard P, Suetta C, Caserotti P, Magnusson SP, Kjaer M. Role of the nervous system in sarcopenia and muscle atrophy with aging: strength training as a countermeasure. Scand J Med Sci Sports. 2010; 20(1): 49-64.
- Deschenes MR. Motor unit and neuromuscular junction remodeling with aging. Curr Aging Sci. 2011; 4(3):209-220.
- Verdu E, Ceballos D, Vilches JJ, Navarro X. Influence of aging on peripheral nerve function and regeneration. J Periph Nerv Syst. 2000; 5:191-208.
- Whiteside MM, Wallhagen MI, Pettengill E. Sensory impairment in older adults: part 2: vision loss. Am J Nursing. 2006; 106(11):52-61.
- Stubbs B, Brefka S, Denkinger MD. What works to prevent falls in community-dwelling older adults? Umbrella review of meta-analyses of randomized controlled trials. Phys Ther. 2015; 95:1095-1110.
- Erickson KI, Leckie RL, Weinstein AM. Physical activity, fitness, and gray matter volume. Neuro BiolAging. 2014; 35:S20-S28.
LeAnn Snow, MD
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