The Neuroarticular Lesion in the Elderly: A Condensed Literature Review

The Aging of the Neuroreceptor Population 

The aging of the neuroreceptor population is seen in the neurarticular complex and related modulating centers associated with reflex and motor control, wherein various neurochemical changes have been observed in the nervous tissue of both aged animals and humans.11 Among the changes noted are alterations in neurotransmitters, their metabolites, and the enzymes involved in their synthesis and degradation. Najlerahim et al11 indicated there was age-related alteration in excitatory amino acid neurotransmission in their animal studies. The hippocampus and cerebellum failed to show significant age-related changes in uptake of D-[3H]aspartate. Uptake of D-[3H]aspartate decreased significantly in the neurocortex (20%), striate nuclei (29%), nucleus basalis (26%), amygdala (19°/a), and thalamus (16%) in the middle-aged rats as compared with young rats, but the changes were not progressive with age. The release of glutamate from the nucleus basalis was unaltered during the aging process. Donzanti and Ung12 report that alterations in neurotransmitter amino acid content in the aging rat striatum are subregionally dependent. These findings demonstrate specific striatal subregional changes in neurotransmitter amino acid content as a function of aging.

In a study by Albert13 on aging epidemiology, it was found that, even among successfully aging, healthy individuals, there is wide variability in structural and functional decline. Test results show, rather conclusively, that there is progressive deterioration in cognitive ability with age related to specific changes in the brain.

This suggests, contrary to what we all were taught, that this is probably not the result of substantial neuronal loss in the cortex. It is more related to specific nuclei where there are changes in neuron numbers with age, such as the basal forebrain, and in changes in synaptic organization, in conductivity, and in neurotransmitter levels that are reflected by these morphologic measurements.13 Humans and other primates show a significant loss in brain weight and an increase in DNA with senescence. By age 80, total brain protein is reduced by 10% to 30%. Concomitantly, there is a progressive increase in total DNA, presumably caused by proliferation of glial cells (gloss), and only a slight increase in water content. Lipid constituents (neural fats, cerebrosides, and phosphatides) decrease minimally with age.14 Age-related alterations in the synthesis and degradation of neurotransmitters and their receptors could explain some of the characteristics of senescence; blood flow to the brain is reduced by 20% in the elderly, which may contribute to the previously mentioned physiologic changes and the following changes in the 70+-year-old group: altered mood, appetite, sleep pattern, neuroendocrine functions, motor activity, and memory.

Chronology of Loss of the Neuroreceptive Field in the Elderly 

Encapsulated receptors, such as Pacini's and Meissner's corpuscles, display age-related changes involving both the capsule as well as the structure of their nerve terminals.15 In a study by Bolton et al,16 it was noted that there was an apparent loss of Meissner's corpuscles from the fingers and toes in the aged population studied. This contributed to significantly less perception to mechanical stimulation on the palms and thumbs in elderly subjects (aged 60 to 70 years) as compared with young individuals (aged 20 to 36 years). In another study by Swash and Fox,17 it was reported that the muscle spindle capsule thickens and there are subsequently fewer intrafusal muscle fibers noted in the elderly. This has significant ramifications relative to the modulation of the gamma intrafusal system and subsequent muscle tonus and the modulation of the central state of the alpha motor neuronal pool. There is a progressive impairment of touch-pressure perception, which approaches a fourfold reduction in males over age 40.18 Postural changes in the elderly have been ascribed to a loss of proprioceptive receptors from ligaments and muscles, leaving primarily visual cues as to the vertical position of the head and neck in space. Regardless of reference to age, it is certain that there is loss of the neuroreceptive field in the elderly and aged population and that this loss may begin as early as age 50.

This age-dependant loss of receptors reduces the ability of the human nervous system to coordinate and interpret the interactions of the individual with his or her environment. The sensory receptors of the nervous system provide a link with the outside world. Neurosensory changes that influence functioning, activities, response to stimuli, and perception of the world do occur with age, and this deficit significantly reduces the protective neuromuscular reflexes of the aged individual.

At the present time, research studies of the articular complex have been conducted primarily postmortem, with the average age of specimens being 60 to 65 years.19 It follows, then, that more should be known about the damaged and diseased motor systems than the normal one. It is precisely because so little is known of normal functional anatomy that problems arise interpreting the data and results of studies of “aging” versus “degeneration.”

Kirkaldy-Willis20 suggests there is considerable evidence to support the point of view that aging and degenerative changes are not synonymous and that degenerative changes do not appear unless the joint has been damaged by trauma of some type. For the most part, joints in healthy active elderly individuals prove to be just as strong in torsion or compression as younger ones.21 Further, degenerated joints appear to be stiffer than normal but fail before healthier ones.22 Pineda et al23 have attempted to develop a histological grading of articular age. These recent studies have demonstrated the development with aging of advanced glycosylated end products (ie, degenerative cross-linked end products of nonenzymatic glycosylation), involving a variety of intracellular and extracellular proteins. Proposed pathogenic mechanisms involving diffuse forms of injury, such as microvascular injury resulting in ganglionic ischemia, would be less favored, because the damage is apparently preferential to selected subpopulations of nerve terminals while sparing others. Both experimental animals and human subjects develop ultrastructural features of neuroaxonal dystrophy involving presynaptic nerve terminals in prevertebral, but not paravertebral, sympathetic ganglia as a function of age.24, 25 Aging in the neuroreceptor population is evidenced by a reduction of about 80% in the number of Meissner's corpuscles between birth and old age; the number of nerves supplying each corpuscle is also reduced; and the nerve endings are confined to the deep end of the core. Interestingly, while the number of Meissner's corpuscles is greatly reduced as one ages, there is also evidence that the Pacincian receptors increase in cell volume as one ages.

The Intervertebral Disk 

No musculoskeletal tissue undergoes more dramatic age-related changes than the intervertebral disk.26 These changes have become even more evident with the use of magnetic resonance (MR) imaging. One of the most common complaints from the elderly person is the reporting of localizing stiffness and discomfort in the back region. This may, in part, be attributed to the aging characteristics of the intervertebral disk.

The increase of collagen cross-links through nonenzymatic glycosylation (glycation) or mechanisms of lipid peroxidation in the intervertebral disk, more importantly, may alter their mechanical properties and contribute to tissue degeneration.27 Age-related defective diffusion mechanism at the vertebral end plate-annular interface provides a basis for the loss of structural integrity of the disk.28 With advancing age, permeability of the end plates decreases.29 The majority of these changes occur within the nucleus pulposus and the transitional region between the nucleus and inner annular fibers near the center of the disk. The collagen of the intervertebral disk not only increases in quantity but also changes in nature. The fibril diameter of collagen in the nucleus pulposus increases, such that the type II collagen of the nucleus starts to resemble the type I collagen of the annulus fibrosus.30 With age, the ratio of keratin sulfate to chondroitin sulfate in the nucleus increases to well above the level found in the annulus.31 Declining nutrition to the chondrocyte population is a critical variable responsible for changes in the cells in the center of the disk and in their matrices.32

Morphologic studies have shown that cell types and the number of viable cells change dramatically with age in the central regions of the disk.33 The fraction of hexosamine in the total dry weight of disk tissue decreases with age, while the collagen content increases in the nucleus.34, 35, 36 Aging chondrocytes change their patterns of synthesis to produce different, more variable matrix proteoglycans.20 Cracking and fissuring of the annular fibers of the intervertebral disk has been demonstrated in young adults. This is accompanied by a loss of the intradiskal water content, as well as a decrease in proteoglycan density. The water content drops from over 85% in preadolescence to about 70% to 75% in middle age.37 This subsequently results in intervertebral disk desiccation and a loss of structural dimensions to include diminished vertical height. This increases the risk for abnormal facet cartilaginous loading. One of the most critical factors in the early decline of the nuclear fiber matrices appears to be that of a progressive malnutrition state near the center of the disk. The cells within the center of the disk matrix are dependent on the passive diffusion of nutrients through the subchondral end plate and from the blood supply at the periphery of the annular fibers. Disorders which may contribute to altered periannular and subchondral blood flow typically seen in the elderly person include vascular disease, chronic smoking, diabetes, and cardiac disease.

Between the second and the seventh decades, the anteroposterior diameter of the lumbar disk increases by about 10% in women and 2% in men, and there is about a 10% decrease in the height of most disks. As well, the upper and lower surfaces of the disk increase in convexity, a change which occurs at the expense of the shape of the vertebral bodies.37 Older lumbar spines show a greater amount of creep and hysteresis, with a greater “set” after creep deformation and a decreased range of motion.38 The greater hysteresis seen in older spines is probably due to the decreased water-binding capacity of the intervertebral disk. Less able to attract water, these disks take longer to resume their original configuration and structure after deformation.39

Vertebral End Plate 

In the subchondral bone of the end plate, vascular channels are gradually occluded, resulting in a decrease in the permeability of the end plate region for nutrients to the disk. Between the ages of 20 and 65, the end plate becomes thinner.40 Moreover, the central portion of the vertebral end plate is rendered more liable to fracture in the presence of excessive compressive loads applied to the disk. Microfractures can be found in the end plates and vertical trabecula of vertebral bodies in greater frequency relative to increasing age.26, 41 Lacking support from the underlying bone, the vertebral end plates deform by microfracture and gradually bow into the vertebral body, imparting a concave shape to the superior and inferior surfaces of the vertebral body.42 With age, the strength of the vertebral end plate decreases and becomes susceptible to compressive loading.43 The vertebral end plates are more likely than the annulus to fail under compression because the tensile strength of the annulus is greater than that of the vertebrae.44

The Zygapophyseal Joints 

During the third decade of life, there is a significant increase in hydration of facet cartilage, which increases more during the fourth decade and remains high throughout adulthood.45 This overall increase in hydration is attributed to the frequent presence of severe fibrillation on the facet joint cartilage after the age of 30 years.45 The articular cartilage and subchondral bone of the anterior, coronal third of the zygapophyseal joint shows changes that are likely to be related to loading of this part of the joint in flexion. The sagittally oriented two thirds of the lumbar joints show age changes which reflect shearing type forces imparted to the articular cartilage through the fibrous capsule.46 Some fibers of the multifidus muscle insert into the fibrous capsule of the zygapophyesal joint. Multifidus atrophy or other pathology will result in abnormal loading characteristics of the facet cartilage surface and contribute to degeneration. Just as abnormal joint stresses produce a characteristic degenerative pathology, lack of joint stress or immobility produces accelerated joint deterioration.47 The effects of stress deprivation on synovial joints are profound, frequently producing intra-articular changes through pannus formation, which nearly obliterate the joint space. If the process is allowed to continue for months, cartilage necrosis is seen in contact areas and erosion/ulceration occur in noncontact areas.45 Intercellular collagen fiber bundles may be decreased in thickness and number secondary to immobilization, ie, atrophy of collagen. Increased joint stiffness after immobilization has been well known clinically and scientifically for decades.47 An overloaded facet joint with a rostrocaudal force will produce a stretching of the joint capsule. Age-related disk space narrowing often results in “settling” or “erosion” of the facet joints.48

Joint Capsules/Ligaments 

Similar to Wolffs49 Law for bones, a generalized statement on the adaptation of applied stress and motion for tendons and ligaments can also be made. Roux50 recognized this “law of functional adaptation” by stating that an organ will adapt itself structurally to an alteration, quantitative or qualitative of function. Therefore, it is not surprising that ligaments are morphologically, biomechanically, and biochemically sensitive to both stress enhancement and stress deprivation.50

In a like manner, age changes (which may be primarily disuse) and repetitive minor trauma bring about substantial loss of resiliency in the joint capsule and ligaments; increasing age also causes ligament “stiffening” as the number of cross-linkages between adjacent collagen fibrils increase substantially, making the fibers less compliant.51 The articular capsule contains mainly fibrocytes or fibroblasts with little ground substance. The aging process leads to diminished articular blood supply51; this relatively poor blood supply yields a slower healing response when zygapophyseal joint capsule damage occurs.52

The tensile properties of some ligamentous-osseous complexes deteriorate markedly with age. Aging is the principal cause of structural changes in ligaments, such as fraying, partial ruptures, necrosis, and cyst formation.53 Specifically, the tensile properties of the ligaments become reduced.54, 55 The subsynovial layer of the articular synovial membrane can be of an areolar, areolar-adipose, fibrous, or fibroareolar matrix. The subsynovial layer is highly vascular and has a plentiful supply of elastin, which imparts a function of elastic recoil during joint movement.56

Loss of Joint Mobility, Denervation, and Atrophy 

Despite the close involvement and relationship between aging, degeneration, and deconditioning, it should be clear that they are not one and the same, although they are inextricably connected. Many anatomic and physiologic experts point out this fact in the previously mentioned research. What is evident is the need for movement and motion even from the cellular level throughout the entire organism. Often the physician is preoccupied with the patient's condition and tends to forget the beginning alteration of structure. With regard to joint and ligament flexibility, the subclinical period of preaffliction is the time when prevention or early intervention is quite effective. When motion is lost, regardless of causation, (ie, degeneration, trauma, inflammation, etc.) movement and biomechanics become of paramount importance to the doctor and patient.

The effect of exercise on age-related muscle atrophy is well documented.6, 57, 58, 59 The active individual can slow the aging processes and often reduce pain-related syndromes.20, 60 The deconditioned, inactive individual will find that the distinction between deconditioning, degeneration, and aging becomes, at times, difficult. By decreasing strength, restricting movement, and causing pain, musculoskeletal impairments prevent people who are middle-aged and older from making full use of their abilities; this limits opportunities for work and impedes the recreational physical activity necessary to maintain optimum mobility for good health. Recognizing this deconditioned state and encouraging an increased activity level will postpone the onset of a multitude of progressive degenerative conditions in the elderly.

Muscle and Motor Unit 

The muscular motor unit undergoes a significant degree of involutional change in the aging population. Myopathic and neuropathic changes can be found in aged muscle.60, 61 The motor unit is the basic functional element of contractile tissue and comprises an alpha-motor neuron, its nerve fiber, and the subserving muscle fibers that it innervates. It has been suggested that there may be trophic interdependence between the alpha motor neuron and its subserving muscle fibers. It is important to keep this in mind when evaluating the motor unit as an aging functional system. The number of motor units decreases with increasing age, especially after mid life.62 The decline in strength in old age reflects decreased numbers of muscle fibers within the motor units.18

There are modest decreases in high-energy metabolites (adenosine diphosphate, adenosine triphosphate, and phosphocreatine) in muscles of the aged.4 Older muscles have an increased susceptibility to contraction-induced mechanical injuries and a decreased ability to regenerate injured tissue. Muscle fiber atrophy, particularly of type II fibers, is a well-documented concomitant of aging; these fibers are fast twitch and anaerobic in metabolic activity.63 It has been suggested that this reflects the changing proportion of a higher percentage of type I to type II fibers in old age.64 Disorganization of myofibrillar architecture, with Z-band “streaming,” may be seen in aging muscle.65

Electromyography of normal elderly persons occasionally shows denervation and reinnervation changes in muscles not subject to entrapment or trauma. These findings are generally attributed to age-related neuronal fallout or subclinical ventral root compression by arthritic vertebrae.66 It is a reasonable hypothesis that maintenance of motor unit populations is a prerequisite for avoiding some of the hazards confronting the elderly, such as bronchopneumonia due to poor lung inflation and accidents due to loss of mobility and disuse.

Even though motor units are lost with age, the increased sizes of the compound action potentials of the surviving units indicate that a proportion of the elderly motoneurons are able to establish collateral reinnervation and to diminish the loss of strength that would otherwise occur. The distal muscles (thenar and extensor digitorum brevis) show losses of motor units with increasing age when investigated by manual estimating techniques.62 The respective declines become statistically significant in the 60- to 79-year-old subjects and are still more marked in the oldest individuals (80 to 98 years). In contrast, the number of motor units appears to be well maintained in the biceps brachii muscle, even in the oldest age group.67

In review, the muscle fibers within a motor unit are of the same type because of the axonal modulated trophic and firing characteristics. Muscle fibers become flaccid and their bulk is reduced secondary to nerve injury with denervation. One of the more obvious, common changes in the motor unit accompanying aging is reduction in bulk. The muscle contours become blunted and rounded, and the total mass decreases from 43% to 25% in senescence.68 Carefully performed studies of both humans and animals show a progressive reduction in muscle fiber size with aging.63

Motor Nerve and Ventral Root 

Segmental demyelination and remyelination in the aged (dog) is particularly evident within the ventral roots.69 Human ventral roots display myelin changes, nerve fiber loss, and an increase in connective tissue with advanced age. Lumbosacral roots are estimated to lose 350 fibers per decade as a consequence of anterior horn cell loss.70 Although there is considerable variation within each decade, axonal counts show a significant decrease in both anterior and posterior roots beginning after age 30; by age 89, a 32% reduction in anterior root axons is observed.71 The ability of motoneurons to sprout and reinnervate denervated muscle is impaired in the aged.72 Experimental studies indicate that a decline in strength in old age reflects both fiber atrophy and a decreased number of muscle fibers.73

Some of the studies on the aging effects on sensory ganglion cells have been contradictory. Some investigators have reported a decrease in the number of cells with age, whereas others have reported no significant depletion. Gardner74 concluded that there is a progressive deposition of lipofuscin within the sensory ganglion cells in the aging population.

The Autonomic Nervous System 

During the aging process, a marked loss of cells occurs in the monoaminergic neuronal systems. This is the region responsible for the regulation of autonomic (vagus, locus coeruleus) and extrapyramidal (substantia nigra) functions.75 The number of sympathetic neuronal cell bodies in the intermediolateral column of the spinal cord diminishes with age.76 A striking depletion of cell bodies has also been reported within the human cervical sympathetic ganglion, although to a lesser degree than other peripheral ganglia such as within the paravertebral ganglia.76

The Speed of Central Processing 

Slowing occurs in such simple motor tasks as running and rate of finger tapping, in sensory perceptions as monitored by latency of sensory evoked response, and in reaction time and more complex tasks requiring central processing.77 The effects of aging are reported to be more marked in complex reaction time tasks, in which the subjects choose between 2 or more alternatives.78 Central decision time is also increased in older subjects asked to mentally rotate geometric figures to determine if they are congruent. Larson et al79 studied the patellar reflex time of healthy males with white-collar jobs aged 25 to 65. He observed a prolongation of the total reflex time, but this was due almost entirely to a delay in the motor time component. The reflex latency, representing the neuronal component, was unchanged.79 Numerous examples have been reported indicating that the more complex the task, the greater the age effect on performance of the task. Birren80 in his studies suggested that these changes reflect a general central nervous system mediated process that impacts across a wide range of behaviors.

Exacerbation in the Deconditioned Patient 

From the foregoing, it is obvious that many factors can cause disturbances in musculoskeletal function. Similarly, degenerative changes associated with the aging neuroarticular complex can lead to loss of compensatory ability and, at times, to disability. This may result from mechanical factors, such as hypertrophic spurs, or developmental anomalies that cause functional spinal problems. Occupational factors, such as repetitive microtrauma on the job or sitting in an incorrect posture at a computer 8 hours a day for years, can also initiate musculoskeletal dysfunction.50 Sudden stress or athletic trauma can also have long-lasting musculoskeletal consequences that manifest as incapacitating symptoms. These considerations lead us to believe that the deconditioned individual is at higher risk of developing degenerative changes within the neurologic complex. Even when aging is apparent, it does not necessarily signal the presence of degenerative neurologic function caused by pathophysiologic causes. Certainly, there are numerous studies to indicate a slowing down of physiologic vigor and function as an aging process; yet, aging is not synonymous with degeneration and dysfunction per se. It is evident from the studies of Lieberman et al81 that substantial differences in the absolute levels and patterns of daily rest and activity were observed across age groups. Overall, the elderly subjects were somewhat more active at times than the young subjects, especially in the early morning. Consistent with their increased levels of daytime activity, the elderly subjects reported less sleepiness and fatigue. These findings suggest that levels and rhythms of daily activity in healthy elderly people are often well preserved and may not deteriorate as readily as had been assumed.

For some individuals, declining mobility leads to loss of independence and the ability to participate in social and recreational interactions with family and friends. Because of the rapid growth in size of the aging population, the need to prevent and treat musculoskeletal disorders among middle-aged and elderly people will increase more than ever before.

Impairments of the musculoskeletal system may result from changes in the bones or soft tissues that form the muscles, articular cartilage, intervertebral disks, tendons, ligaments, and joint capsules. Fractures associated with age-related alterations in bone cause severe morbidity and, in some cases, mortality; however, they do not cause impairment for as many older people as do weakness, pain with movement, and restriction of motion caused by changes in the soft tissues.82 Although any part of the musculoskeletal system may be affected, the back and the lower extremities are the most frequently reported locations of musculoskeletal impairment. In addition to the decrease in musculoskeletal function caused by the development of age-related degenerative disorders, loss of tissue strength with age83 may increase the probability or severity of soft tissue damage from a given trauma.

Recent research has shown that degenerative changes after tissue insult do not progress uniformly and that intervention may alter their progression.81 Thus, there is a clear need to disseminate knowledge of the basic processes of aging and the methods for maintaining and improving musculoskeletal function in older individuals, both as a preventative measure and as an element in the care of the deconditioned patient.

Although loss of skeletal muscle mass and declining strength with age appear to be inevitable, a number of variables may slow these changes. Many investigators have found convincing evidence that exercise increases the strength of older individuals by increasing muscle mass, cross-sectional areas, contractile proteins, motor unit recruitment, and oxidative capacity of the muscular system. Exercise improves other aspects of the aging individual's life, such as confidence performing activity requiring some agility.

Postural Changes Associated with Aging 

Posture can be defined as the relationship of each body structure to the entire structure. The observed increase in the US older adult population (older than 65) is associated with a rise in the number of members of this population participating in athletic activities.84 Although postural dyscontrol is associated with the older adult population, it may be a byproduct not necessarily of the aging process but rather of sedentary lifestyle; physical activity appears to play a key role in maintaining good postural control.85

Schafer86 reports that anatomists and neurophysiologists no longer question the significance of the entire proprioceptive and neuroreceptor distribution in the ligamentous and myologic elements of the spine and pelvis when considering dynamic or static posture. Evidence suggests that the interplay between curvature and the ligaments that maintain it imparts a resilience that is important in protecting the vertebral column against excessive compressive forces and strains that may be encountered in various postures and during movement. It has been noted that some cases of back pain are attributable to abnormal posture or marked alterations of the curve.87 Earlier studies by Allbrook40 and Erickson88, 89 showed that there were significant changes in the dimensions of the lumbar vertebral bodies with age. Histologic studies83, 90 have clarified that the iliolumbar ligamentous apparatus and sacroiliac ligamentous apparatus, which play an important role in the mechanics of the lumbosacral junction, undergo extensive morphologic changes from birth to maturity, resulting in marked transformation of its structure and presumably its functional characteristics affecting posture.

The concept of a generalized aging effect on posture and the balance mechanism has been identified and discussed by a number of researchers.91 Neurophysiologic models of sensorimotor control of posture and movement are evolving rapidly. Because postural instability is so common in the aged population group, it is considered by one model as an inevitable aging effect resulting from widespread degeneration of the musculoskeletal, neuromuscular, and sensory systems.

Postural control requires the ability to correctly predict, as well as detect and encode, the characteristics of any active or passive disturbance in posture. In unusual sensory environments, this may require selecting the most reliable source of sensory information available from the mechanoreceptors. Postural control also requires the ability to select and finely adapt a corrective or protective response and to execute that response within the biomechanical constraints of the body and the physical constraints of the environment.

The proper postural neuroreceptive field will depend on the individuals' ability to select an appropriate postural response, to match the magnitude of the response to the magnitude of the disturbance, and to execute the chosen response quickly and effectively. Thus, any disruption in the ability to coordinate and move muscles and joints effectively and efficiently must necessarily compromise postural stability.91 Because patterns of neural activity from the central nervous system must be implemented by the body's musculoskeletal system, postural stability is necessarily constrained by the body's biomechanics, including joint mobility and the distribution and quality of muscle strength. Although postural control may be divided into motor and sensory components, it is clear that posture is a complex feedforward reflex mechanism requiring intact receptors and sufficient muscle fiber density for control.

When the body is traumatized, internal and/or external stress factors will involve the nervous system, directly or indirectly, resulting in decreased mobility of the vertebrae of the involved neuroarticular complex. This decreased mobility may be the result of muscle splinting, especially on the side of greatest stimulation according to Pfluger's Law5 or from abnormal weight distribution to the superior facets and other structures of the vertebrae involved.

Pfluger's Law5 states that, if a stimulus received by a sensory nerve extends to a motor nerve of the opposite side, contraction occurs only from corresponding muscles, and if contraction is unequal bilaterally, the stronger contraction always takes place on the side that is stimulated. When affecting 1 or more vertebrae, this state of decreased mobility of the motion unit encourages neuronal dysfunction leading to pathologic alterations in the area supplied by the neurocomplex. Depending on the degree and chronicity of involvement, these may or may not lead to a manifestation of the degenerative process. Palpable alterations of the normal anatomic relationships of one joint to another are frequently found. These mechanical changes may occur in the static recumbent, sitting, or standing positions, as related to the various ranges of motion the spine and its individual segments are put through during daily activity.

Prolonged immobilization such as occurs in posttraumatic support or disuse may lead to greatly diminished joint lubrication, as well as atrophy of muscle, cartilage, and subcutaneous fat, along with chronic circulation disturbances, capsular contraction, and bone decalcification. Gozna and Harrington,92 in their description of the biomechanics of musculoskeletal injury, describe this clinical picture in detail.

Both degenerative processes and aging factors may contribute to functional and postural changes that occur at the articular complex. Aging decreases articular cartilage permeability up to the age of about 40, after which an increase in permeability begins to develop.92 However, aging has little or no influence on the elastic properties of articular cartilage, while its effect on tensile strength is as yet unknown. Microtrauma and/or macrotrauma with inflammation will increase the permeability of synovial vessels, thus allowing influx of plasma that will adversely alter the joint's mechanical properties. Any joint fixation or subluxation will produce abnormal unilateral loads which tend to break down articular cartilage.93 Even in a well-lubricated joint with continuous immobilization in a forced position, chondrocytes will die and degenerative arthritis will be encouraged. Its extent, from superficial to deep involvement, is proportional to the duration of the “fixation compression.” In addition, the protein polysaccharide complexes become depleted. The cartilage becomes unable to withstand stress as movement occurs and degenerative, sometimes painful changes develop. This invariably sets the stage for alterations in the neuroarticular complex, as well as a habitual postural imbalance caused by the adaptive mechanism secondary to this degenerative process.

Postural changes then may be the result of gross structural alterations that may become neuropathologic with age. Yet, as was stated earlier, aging does not necessarily mean a neuropathologic status of the individual.