Journal of Gerontological Nursing

Aging and Memory Loss

Joseph P Maloney, RN, PhD, LTC, ANC; Claudia Bartz, RN, MN, ANC

Abstract

Introduction

Memory is an integral part of the human organism. It is that aspect of adaptation that makes one sentient, responsive, and interactional. The awareness and cognizance of that consciousness are structured by memory, by a recognition of one's own responses. Loss of memory causes diminished consciousness with loss of psychological and social self. With severe memory loss, a person loses any vestige of a meaningful life; the individual's capacity to maintain homeostasis and to meet the challenges of a changing world deteriorate and, even before biologic death, the conscious person is converted into a vegetative organism.'

Decrement in memory is a component of the aging process. A decrease in shortterm memory, which is a decrease in the ability to acquire and retain information, is characteristic of the aging individual. Commonly, an older person easily recalls past events and people with acuity for dates and details, but has trouble remembering the contents of breakfast that very morning. Popular and scientific 'opinion apparently are compatible with respect to the pattern of age-dependent memory ability.

Although significant declines in memory may have been overestimated in earlier cross-sectional studies, there is increasing evidence based on more carefully controlled longitudinal studies that memory decrements are inevitable even in normal aging.2

The problem of memory loss in later life is important because many cognitive, perceptual, and personality dimensions are changed with the loss. For example, decreased awareness, with consequent self-doubt and lowered selfesteem, may alter or eliminate the societal contacts that are essential to life.

What, then, is "normal" memory loss with aging? What are the pathological changes in an aging brain? This paper seeks to answer these questions and, further, to present a discussion of the potentially crucial physiological role of the hippocampus in short-term memory. This psychophysiological approach may aid those responsible for dealing with the aged, whether in a social or a professional role.

Normal Memory Loss with Aging

The Process of Memory

Memory is a complex phenomenon and it would not be surprising to find that it is mediated by a variety of information-handling processes. Accordingly, such processes would be activated in a variety of different ways, depending on the nature and amount of information to be committed to memory.

The study of memory has generated a number of competing theories that relate to the processes involved in human memory. According to Craik,3 the most widely-accepted theory of memory today is the three-stage model of memory: 1) sensory or primary memory stage, 2) short-term or secondary memory stage, and 3) long-term or tertiary memory stage. This view presents a clear and workable basis for describing memory.

Sensory or Primary Memory Stage. If a person is given a five digit number and immediately is asked to repeat the number, that person can do so by reading out the c*ontents of what psychologists usually term "primary memory."4 The capacity of the primary memory is limited to only a few items; information seems to decay rather rapidly from primary memory unless rehearsed. The time taken to recall items from primary memory is somewhat longer with older subjects,5 but the number of items that can be held and retrieved from primary memory is related very minimally to age.6 Loss of primary"memory capacity is not the type of loss that older people typically experience.

Short-Term or Secondary Memory Stage. If a person crams a list of 30 vocabulary words 15 minutes prior to an exam and then manages to write the words on the exam, the person has recalled information from "secondary memory." Remembering to buy eight particular items at the grocery store on the way…

Introduction

Memory is an integral part of the human organism. It is that aspect of adaptation that makes one sentient, responsive, and interactional. The awareness and cognizance of that consciousness are structured by memory, by a recognition of one's own responses. Loss of memory causes diminished consciousness with loss of psychological and social self. With severe memory loss, a person loses any vestige of a meaningful life; the individual's capacity to maintain homeostasis and to meet the challenges of a changing world deteriorate and, even before biologic death, the conscious person is converted into a vegetative organism.'

Decrement in memory is a component of the aging process. A decrease in shortterm memory, which is a decrease in the ability to acquire and retain information, is characteristic of the aging individual. Commonly, an older person easily recalls past events and people with acuity for dates and details, but has trouble remembering the contents of breakfast that very morning. Popular and scientific 'opinion apparently are compatible with respect to the pattern of age-dependent memory ability.

Although significant declines in memory may have been overestimated in earlier cross-sectional studies, there is increasing evidence based on more carefully controlled longitudinal studies that memory decrements are inevitable even in normal aging.2

The problem of memory loss in later life is important because many cognitive, perceptual, and personality dimensions are changed with the loss. For example, decreased awareness, with consequent self-doubt and lowered selfesteem, may alter or eliminate the societal contacts that are essential to life.

What, then, is "normal" memory loss with aging? What are the pathological changes in an aging brain? This paper seeks to answer these questions and, further, to present a discussion of the potentially crucial physiological role of the hippocampus in short-term memory. This psychophysiological approach may aid those responsible for dealing with the aged, whether in a social or a professional role.

Normal Memory Loss with Aging

The Process of Memory

Memory is a complex phenomenon and it would not be surprising to find that it is mediated by a variety of information-handling processes. Accordingly, such processes would be activated in a variety of different ways, depending on the nature and amount of information to be committed to memory.

The study of memory has generated a number of competing theories that relate to the processes involved in human memory. According to Craik,3 the most widely-accepted theory of memory today is the three-stage model of memory: 1) sensory or primary memory stage, 2) short-term or secondary memory stage, and 3) long-term or tertiary memory stage. This view presents a clear and workable basis for describing memory.

Sensory or Primary Memory Stage. If a person is given a five digit number and immediately is asked to repeat the number, that person can do so by reading out the c*ontents of what psychologists usually term "primary memory."4 The capacity of the primary memory is limited to only a few items; information seems to decay rather rapidly from primary memory unless rehearsed. The time taken to recall items from primary memory is somewhat longer with older subjects,5 but the number of items that can be held and retrieved from primary memory is related very minimally to age.6 Loss of primary"memory capacity is not the type of loss that older people typically experience.

Short-Term or Secondary Memory Stage. If a person crams a list of 30 vocabulary words 15 minutes prior to an exam and then manages to write the words on the exam, the person has recalled information from "secondary memory." Remembering to buy eight particular items at the grocery store on the way home from work also exemplifies this type of memory. Secondary memory is only a semi-permanent storage bank.

Secondary memory is lost during the aging process.7'8 Older subjects not only have difficulty with attempts to recall material but also take longer and make more errors when asked to decide whether a given item is in a memorized list.3

In addition to particular difficulties with information storage or retrieval, Eisdorfer9 has stated that older subjects may not perform well on secondary memory tasks due to their decreased motivation to recall recent events. Nevertheless, he also points out that motivational differences seem quite unlikely as a basis for the total agerelated differences found in secondary memory capacity.

Long-Term or Tertiary Memory Stage. In contrast to the age-related deficit of secondary (short-term) memory, the person's store of long-held knowledge, tertiary memory, seems to change little with age. Except in cases of definite pathology, a person's motor skills, language habits, and memory for remote experiences seem to remain unchanged throughout the life cycle.10 Laboratory studies indicate that the time required to retrieve a name from tertiary memory increases slightly with age. However, the age-related increase in retrieval time from tertiary memory is far less than the increase in time needed to retrieve items from secondary memory.11

Sociological Factors in Memory Loss

It is tempting to classify the memory decrement that occurs with age as part of the normal, inevitable, geneticallydetermined continuum that leads to senility and, finally, to death. However, the normal decline in mental functional capacity may not progress to recognizable cognitive impairment unless the functional brain receives specific accelerants to its loss. The accerlerants could be illness, physical impairment, or unidentified factors that lead to damage of brain cells.12

Botwinick" has observed that it is difficult to assess scientifically what normally happens to memory as aging takes place. For example, after the age of 80, memory declines less in men than in women. This may be because those men who have survived are the stalwarts; men of lesser strength and ability have died by then. The lower women's death rate at all ages may serve to defer the demise of the older woman with poor memory.

Older persons of higher social class, whether mentally normal or mentally impaired, were found to have better memories in old age than did those older persons with less education and lower occupational status. Level of intelligence also was found to be related directly to memory in later life.1

Studying the effects of genetic factors and environmental influences on shortterm memory capacities of older persons is a multivariable task. In spite of the difficulties, further study may illuminate methods for the delay or prevention of short-term memory loss in the elderly.

Pathology of the Aging Brain

Early studies of the pathogenesis of memory deficits in the aging population focused on cerebral blood flow with cerebrovascular insufficiency, nerve cell loss postulated as being insufficiency, and nerve cell loss postulated as being the primary cause of the memory loss. Kety13 and Gottstein14 reported observations of age-related decline in cerebral blood flow and decrease in oxygen and glucose consumption. Brody15 reported observations of age-related decline in cerebral blood flow and decrease in oxygen and glucose consumption. Brody15 suggested an irreversible loss of neurons in the aging brain on the basis of decreasing brain weight.

Drugs such as potassium iodide, glutamic acid, and magnesium pemoline have been used in attempts to counter cerebrovascular insufficiency with little success. Drug groups including RNA substances, amphetamines, and antioxidents also have been used in the aged with memory loss, but with no apparent reversal of the cognitive defects. Hyperbaric oxygenation has been studied to identify its potential for maintenance of the brain's functions, but it has not yet proven to be of any value in increasing capacity for memory.1

More recently, studies have established that many patients showing signs of mental decline often will have normal blood vessels on autopsy.16'" Goldfarb and Austin'8 were unable to demonstrate that stroke or arteriosclerosis were responsible for a decline in the ability to remember. Victor" reported that a patient with bilateral cerebral infarctions in the location of the posterior cerebral arteries was found to have a striking impairment of short-term memory. The patient's long-term memory was not affected. On autopsy, the brain of this patient was found to have extensive infarction of the left temporal lobe, particularly the hippocampus and the hippocampal gyrus.

The aging brain exhibits a characteristic pattern of histopathologicchanges. With advancing age, there is a slight decrease in the number of cortical neurons. However, precise morphometry studies have reported a relatively constant neuronal weight with increasing age. Lipofuscin normally accumulates in neurons in increasing amounts with age. Senile plaques, Alzheimer's neurofibrillary changes, and granulovascular degeneration also are observed. Most of the changes in the human brain tissue normally occur in the cortical tissue, particularly in the simple cortex of the hippocampal complex.20

The Hippocampus and Short-Term Memory

Considering histological changes that are evident in the aging brain, studies of the hippocampus in humans, and disease entities that involve the hippocampus, the hippocampus apparently is the center for short-term memory.

Physiology of the Hippocampus

The hippocampus is an elongated structure composed of a modified type of cerebral cortex that has been folded inward to form the ventral surface of the inferior horn of the lateral ventricle. One end of the hippocampus lies immediately adjacent to the amygdaloid nuclei and also fuses along one of its borders with the hippocampal gyrus, which is the cortex of the ventromedial surface of the temporal lobe.21

The hippocampal complex is a very intricate system of circuits. The hippocampal afferents relay to the anterior thalamic nuclear complex where they interact with afferents entering via the mamillary bodies of the hypothalamus. Limbic projections to the mamillary body may represent feedback loops to that structure carrying information about higher limbic states of activity."

Studies of the Hippocampus in Humans

Terzian and Dalle Ore23 reported memory disturbances in a man who had undergone a two-stage bilateral temporal lobectomy as treatment for uncontrolled psychomotor epilepsy. The patient had severe deficit for recent (shortterm) memory, spotty deficits for longterm memory, and was unable to learn new information.

In 1957, Scoville and Milner24 reported profound defects of recent memory after bilateral resection of the hippocampus in a patient identified as H.M. Since Scoville and Milner's original report, H.M. has been studied extensively in order to delineate the qualitative and quantitative characteristics of his hippocampal memory disorder. The patient consistently has demonstrated a very severe deficit for recent memory and a somewhat lesser deficit for long-term memory, but no intellectual decline.25'26 Other cases reported by Milner and associates clearly have established the importance of the hippocampus in human memory, especially short-term memory.27-29

Disease Entities Involving the Hippocampus

Korsakoff's Syndrome. The clinical symptoms of Korsakoff's Syndrome as it occurs in an alcoholic have been known for some time. Pathologically, there is damage to the mamillary bodies or to the nucleus medialis dorsalis, or to both. These structures are associated anatomically with the hippocampus and with the limbic system. Clinically, the individual has deficits in both shortterm and long-term memory.22

Senile Dementia of the Alzheimer's Type (SDAT). This disease often is referred to in the literature as primary neuronal degeneration of the Alzheimer's type. It is a cortical disease of, as yet, unknown etiology that occurs in the 40-to-50-year-old age group. Clinically, the disease resembles senile dementia seen in older people; its earliest features are impaired memory and difficulty with problem solving. The memory loss is most obvious in the short-term memory stage. Pathologically, these characteristic features are seen with increasing frequency in persons diagnosed as having Alzheimer's disease. Most significant are the senile plaques and collection of argyrophilic granular material that are seen to the greatest extent in the hippocampus.30

Summary

An important problem of the aging individual is a decrement in short-term memory. With this gradual loss, the person loses his or her ability to maintain contact with the environment. Failure to meet the constant demands for cognition and perception causes the aging person to develop diminished self-awareness, decreased self-esteem, and, perhaps, a pathological state of consciousne..

The health professional requires a sound psychophysiological basis for working with the aging population in health maintenance and in treatment of illness or disease. Further study is needed of the sociological factors that affect and determine one's capacity for short-term memory. More evaluation of the pathological changes that occur in the brain with aging also is needed. Studies of the role of the hippocampus in human short-term memory indeed may provide a rational and scientific approach to treatment and prevention of short-term memory loss in the aging population.

References

  • 1. Goldman R, Rockstein M: The Physiology and Pathology of Human Aging. New York, Academic Press. 1975.
  • 2. Birren JE, Schaie KW (eds): Handbook of the Psychology of Aging, vol 2. New York, Van Nostrand Reinhold Co, 1977.
  • 3. Craik FIM: Age differences in human memory. In Birren J, Schaie KW (eds): Handbook of the Psychology of Aging. New York, Van Nostrand Reinhold, Co, 1977.
  • 4. Schwartz AN, Peterson JA: Introduction to Gerontology. New York, Holt, Rinehart 8c Winston, 1979.
  • 5. Waugh K: Recalling names from primary and secondary memory. Gerontologist 12:54-58, 1972.
  • 6. Arenberg D; The effects of input condition on free recall in young and old adults. J Gerontol 31:551-555, 1976.
  • 7. Walsh, D. Age differences in learning and memory. In Woodruff DS, Birren JE (eds): Aging. New York, Van Nostrand Co, 1975.
  • 8. Eysenck MW: Age differences in incidental learning. Developmental Psychology 10:936-941, 1974.
  • 9. Eisdorfer C, Nowling J, Wilkie R: Improvement of learning in the aged by modification of autonomic nervous system activity. Science 170:1327-1329, 1970.
  • 10. Botwinick J, Sturandt M: Memory, Related Functions and Age. Springfield, IL; Charles C. Thomas, 1974.
  • 11. Botwinick J: Aging and Behavior. New York, Springer Publishing Co, 1978.
  • 12. Gaitz CM (ed): Aging and the Brain New York, Plenum Press;-1972.
  • 13. Kety SS: Blood flow and metabolism of the human brain in health and disease. J Chronic Dis 3:459-477, 1955.
  • 14. Gottstein U: Pharmacological studies of total cerebral blood flow in man with comments of the possibility of improving regional cerebral blood How by drugs. Acta Neurologica Scanüinavica 41:136-141, 1965.
  • 15. Brody H: Organization of the cerebral cortex. / Comp Neurol 102:511-516, 1955.
  • 16. Baker AB, Parker HH: Clinical Neurology. Maryland, Harper and Row, 1974.
  • 17. Peress NS. Kane WC, Aronson SM: Central nervous system findings in the tenth decade autopsy population. Prog Brain Res 40:473-483, 1973.
  • 18. Goldfarb AI, Austin S: Unpublished data. In Goldman R, Rockstein M (eds): The Physiology and Pathology of Human Aging. New York. Academic Press, 1975.
  • 19. Victor M: Observation of the amnesic syndrome in man and its anatomical basis. In Brazier M (ed): Brain Function. Los Angeles, University of California Press, 1964.
  • 20. Barbagallo-Sangiorgi G, Exton-Smith A: The Aging Brain: Neurological and Mental Disturbances. New York, Plenum Press, 1980.
  • 21. Guy ton AC: Textbook of Medical Physiology, ed 4. Philadelphia, WB Saunders Company. 1980.
  • 22. Issacson R, Pribram K: The Hippocampus. New York, Plenum Press. 1975.
  • 23. Terzian H, Dalle Ore G: Syndrome of Kluver and Buey reproduced in many by bilateral removal of the temporal lobes. Neurology 5:373-380, 1955.
  • 24. Scoville WB, Milner B: Loss of recent memory after bilateral hippocampal lesions. J Neurol Neurosurg Psychiatry 20:11-21, 1957.
  • 25. Prisko L: Short-term memory in focal cerebral damage. Arch Neurol 13:52-62, 1963.
  • 26. Sidman M, Stoddard LT. Mohr JP: Some additional quantitative observations of immediate memory in a patient with bilateral hippocampal lesions. Neuropsychologia 6:245-254, 1965.
  • 27. Milner B: Amnesia following operations on the temporal lobes. In Whitty CWM, Zangwill OL (eds): Amnesia. London, Butterworths, 1966.
  • 28. Milner B: Memory and the medial temporal regions of the brain. In Pribram KH, Broadbent DE (eds): Biology of Memory. New York, Academic Press, 1970.
  • 29. Penfield W, Milner B: Memory deficit produced by bilateral lesions in the hippocampal zones. Archives of Neurology and Psychiatry 79:475, 1958.
  • 30. Terry RD: Structural changes in senile dementia of the Alzheimer type. In Atnaducci L. Davison A. Antuotio P (eds): Aging of the Brain and Dementia (Aging, vol 13.) New York, Raven Press, 1980.

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