Danse-thérapie et Parkinson

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Movement disorders and normal aging

Identifieur interne : 000016 ( Istex/Corpus ); précédent : 000015; suivant : 000017

Movement disorders and normal aging

Auteurs : Padma R. Mahant ; Mark A. Stacy

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DOI: 10.1016/S0733-8619(05)70034-7

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<note>Address reprint requests to, Mark A. Stacy, MD, Muhammad Ali Parkinson Research Center, 500 W. Thomas Avenue, Suite 700, Phoenix, AZ 85013</note>
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<ce:note-para>Address reprint requests to, Mark A. Stacy, MD, Muhammad Ali Parkinson Research Center, 500 W. Thomas Avenue, Suite 700, Phoenix, AZ 85013</ce:note-para>
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<ce:dochead>
<ce:textfn>Movement Disorders and Normal Aging</ce:textfn>
</ce:dochead>
<ce:title>Movement disorders and normal aging</ce:title>
<ce:author-group>
<ce:author>
<ce:given-name>Padma R.</ce:given-name>
<ce:surname>Mahant</ce:surname>
<ce:degrees>MD</ce:degrees>
</ce:author>
<ce:author>
<ce:given-name>Mark A.</ce:given-name>
<ce:surname>Stacy</ce:surname>
<ce:degrees>MD</ce:degrees>
</ce:author>
<ce:affiliation>
<ce:textfn>From the Movement Disorders, Muhammad Ali Parkinson Research Center at Barrow Neurological Institute, Phoenix, Arizona</ce:textfn>
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<ce:sections>
<ce:para>Movement disorders are particularly prevalent in the elderly. Disorders of gait and mobility are second only to cognitive impairment as the most frequent neurologic effects of aging.
<ce:cross-ref refid="bib40">
<ce:sup>40</ce:sup>
</ce:cross-ref>
In 1998, there were 34.4 million Americans over the age of 65,
<ce:cross-ref refid="bib80">
<ce:sup>80</ce:sup>
</ce:cross-ref>
and the United States Census Bureau projects that by the middle of the century the population of persons 65 years and over will reach 80 million.
<ce:cross-ref refid="bib79">
<ce:sup>79</ce:sup>
</ce:cross-ref>
In addition, the rate of elderly population growth is more rapid in developing countries than in developed countries.
<ce:cross-ref refid="bib79">
<ce:sup>79</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>As the proportion of Americans over the age of 65 increases from one in eight to one in five by 2030,
<ce:cross-ref refid="bib79">
<ce:sup>79</ce:sup>
</ce:cross-ref>
it is important for clinicians to be able to recognize the effects of normal aging. Furthermore, it is essential to distinguish age–related changes from diseases that accompany aging. The influence of normal aging on the evaluation of major hypokinetic and hyperkinetic movement disorders, including Parkinson's disease (PD) and essential tremor (ET), will be discussed.</ce:para>
<ce:section id="cesec1">
<ce:section-title>The Basis of Motor Impairment in Normal Aging</ce:section-title>
<ce:para>Age–related anatomic and pathologic changes in older adults consist of loss of volume in cerebral hemispheres, diminution of brain weight, gyral atrophy, ventricular dilatation, and decreased cortical thickness.
<ce:cross-refs refid="bib12 bib67 bib76">
<ce:sup>12,67,76</ce:sup>
</ce:cross-refs>
Shrinkage of large neurons predominates, resulting in an increase in small neurons and glia, particularly in the midfrontal and superior temporal cortices.
<ce:cross-ref refid="bib76">
<ce:sup>76</ce:sup>
</ce:cross-ref>
Cerebellar atrophy has been demonstrated in normal aging as well.
<ce:cross-ref refid="bib35">
<ce:sup>35</ce:sup>
</ce:cross-ref>
Regional cerebral blood flow, measured by Xenon CT scanning, declines in the elderly, particularly in the prefrontal, parietal, inferior temporal, frontotemporal regions, as well as the subcortical gray matter of the thalamus, putamen, and caudate.
<ce:cross-ref refid="bib47">
<ce:sup>47</ce:sup>
</ce:cross-ref>
This decline may reflect a higher prevalence of arteriosclerotic changes in the elderly, or age–related declines in metabolic demands of the brain.
<ce:cross-ref refid="bib47">
<ce:sup>47</ce:sup>
</ce:cross-ref>
FDG–PET has been used to explore metabolic topography of normal aging, and frontal, specifically premotor cortex, hypometabolism has been demonstrated.
<ce:cross-ref refid="bib49">
<ce:sup>49</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>Anatomic and pathologic changes that affect dopaminergic function have been widely studied in PD and normal aging. In both instances, the width of the substantia nigra pars compacta, as measured by MRI, is directly associated with motor function.
<ce:cross-ref refid="bib59">
<ce:sup>59</ce:sup>
</ce:cross-ref>
In normal aging, this decline is correlated with poor performance on motor tasks; in PD patients, the reduction in substentia nigra pars compacta width is associated with poor motor performance and higher UPDRS motor scores.
<ce:cross-ref refid="bib59">
<ce:sup>59</ce:sup>
</ce:cross-ref>
Furthermore, autopsy review has demonstrated an age–related loss of neurons in the zona compacta of the substantia nigra of approximately 6% per year.
<ce:cross-ref refid="bib46">
<ce:sup>46</ce:sup>
</ce:cross-ref>
The pathologic changes in normal aging and PD, although similar, should not be considered equivalent; Kish et al have estimated that the 80%–90% striatal dopamine loss necessary to develop parkinsonism would not occur in an individual with normal age–related dopamine decline until the age of 110, far beyond the current average life expectancy.
<ce:cross-ref refid="bib32">
<ce:sup>32</ce:sup>
</ce:cross-ref>
In addition, the pattern of dopamine loss observed in the putamen and caudate is uniform in normal aging, while putamenal loss is more severe in PD.
<ce:cross-ref refid="bib32">
<ce:sup>32</ce:sup>
</ce:cross-ref>
Although the mechanism of cell loss in normal aging is unknown, apoptosis, with nuclear and cytoplasmic shrinkage and aggregation of neuromelanin, similar to the cell death observed in PD, has been demonstrated.
<ce:cross-ref refid="bib78">
<ce:sup>78</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>Neurochemical alterations specifically affecting dopaminergic function are also known to occur with aging. Severe loss of striatal tyrosine hydroxylase, the rate-controlling enzyme in the synthesis of dopamine, as well as dopamine transporters, vesicular monoamine transporters, and D2 receptors have been demonstrated.
<ce:cross-refs refid="bib13 bib46 bib58">
<ce:sup>13,46,58</ce:sup>
</ce:cross-refs>
Monoamine oxidase (MAO) has been shown to be consistently elevated in the frontal cortex, striatum, globus pallidus, and substantia nigra pars compacta in normal elderly subjects.
<ce:cross-refs refid="bib13 bib72">
<ce:sup>13,72</ce:sup>
</ce:cross-refs>
Increased MAO may hasten degradation of dopamine and norepinephrine to produce elevated concentrations of monoamine catabolites reported in the cerebrospinal fluid of elderly patients.
<ce:cross-ref refid="bib72">
<ce:sup>72</ce:sup>
</ce:cross-ref>
</ce:para>
</ce:section>
<ce:section id="cesec2">
<ce:section-title>Clinical Manifestations of Normal Aging</ce:section-title>
<ce:para>The neurochemical, neuroanatomic, and neuropathologic changes that occur in normal aging impart gradual declines in cognition, motor function, sensation, coordination, balance, and ambulation. The aggregation of these changes, which are further magnified by impaired integration of these systems, results in the picture of declining mobility in the elderly.</ce:para>
<ce:para>Frontal lobe dysfunction has been postulated to explain the decline in visuospatial perception, information processing, and reaction speed associated with both aging and PD.
<ce:cross-refs refid="bib5 bib10 bib11 bib20 bib48 bib49 bib56 bib63 bib67">
<ce:sup>5,10,11,20,48,49,56,63,67</ce:sup>
</ce:cross-refs>
Fozard et al studied reaction times to auditory stimuli as part of the Baltimore Longitudinal Study of Aging, and found that reaction time increases at a rate of 0.5–1.6 milliseconds (ms) per year, starting at age 20. In this paradigm the mean simple reaction time of 225 ms in the second decade increases to 273 ms by the eighth decade.
<ce:cross-ref refid="bib17">
<ce:sup>17</ce:sup>
</ce:cross-ref>
Simple reaction times in PD patients are significantly slower than reaction times in healthy controls. Wang et al have estimated a slowing of 34% in PD patients compared with healthy controls.
<ce:cross-ref refid="bib82">
<ce:sup>82</ce:sup>
</ce:cross-ref>
Slower simple reaction times in PD patients have been linked to difficulty with preprogramming of motor responses, and the premotor, supplementary cortex has been implicated in this deficit.
<ce:cross-ref refid="bib7">
<ce:sup>7</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>Oculomotor dysfunction, in particular vertical gaze palsy, is seen in several movement disorders, including PD and progressive supranuclear palsy.
<ce:cross-ref refid="bib61">
<ce:sup>61</ce:sup>
</ce:cross-ref>
Kaye et al used standardized criteria for testing eye movements to find significant declines in upgaze, pursuit, and saccadic function with aging.
<ce:cross-ref refid="bib30">
<ce:sup>30</ce:sup>
</ce:cross-ref>
The average limitation in upgaze of 5.9% in otherwise normal subjects ages 65 to 74 increased to 64.7% in those over 84 years.
<ce:cross-ref refid="bib30">
<ce:sup>30</ce:sup>
</ce:cross-ref>
Others have reported vertical gaze impairment in approximately 30% of individuals in the eighth decade of life.
<ce:cross-ref refid="bib29">
<ce:sup>29</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>Motor examination often reveals muscle atrophy, increased tone, reduced power, and declining motor speed in the elderly population. In addition, musculoskeletal abnormalities in the elderly may result in focal pain and mechanical restriction of movement, which may be mistaken for bradykinesia.
<ce:cross-refs refid="bib50 bib61">
<ce:sup>50,61</ce:sup>
</ce:cross-refs>
A community population study by Bennet et al revealed lower extremity rigidity in approximately 45% of individuals over the age of 85.
<ce:cross-ref refid="bib4">
<ce:sup>4</ce:sup>
</ce:cross-ref>
The increased tone generally takes the form of paratonic rigidity, which is described as progressively increased or irregular resistance to passive movement.
<ce:cross-ref refid="bib61">
<ce:sup>61</ce:sup>
</ce:cross-ref>
Potvin et al have demonstrated a decrease in power from 21% to 45% in arms and legs when comparing subjects ages 20 to 80.
<ce:cross-ref refid="bib57">
<ce:sup>57</ce:sup>
</ce:cross-ref>
Hand and foot speeds also declined from ages 20 to 80, as demonstrated by hand tapping and step tracking movement.
<ce:cross-ref refid="bib57">
<ce:sup>57</ce:sup>
</ce:cross-ref>
Testing of coordination tasks in this same population revealed a 14%–27% decline in performance on various coordination tests, such as inter-finger manipulation, finger grasping and progressive arm tracking.
<ce:cross-ref refid="bib57">
<ce:sup>57</ce:sup>
</ce:cross-ref>
Additionally, testing of simulated activities of daily living revealed an average loss in function of 30% from ages 20 to 80.
<ce:cross-ref refid="bib57">
<ce:sup>57</ce:sup>
</ce:cross-ref>
These activities included managing small and large buttons, manipulating safety pins, zipping garments, tying bows, rotating pegs, handwriting speed, and cutting with a knife.
<ce:cross-ref refid="bib57">
<ce:sup>57</ce:sup>
</ce:cross-ref>
Similar complaints are noted by patients with PD.</ce:para>
<ce:para>Electromyographic studies in the elderly have revealed increases in amplitude, duration, and complexity of motor unit action potentials, indicative of increasing motor unit size; this may reflect age–related denervation with compensatory reinnervation, loss of anterior horn motor cells, or degeneration of anterior spinal roots or peripheral motor nerves.
<ce:cross-ref refid="bib24">
<ce:sup>24</ce:sup>
</ce:cross-ref>
Furthermore, decreased motor unit firing rates have been described, suggesting age–related changes in upper motor neuron function or central drive.
<ce:cross-ref refid="bib24">
<ce:sup>24</ce:sup>
</ce:cross-ref>
Motor control laboratories have reported decreased end–point accuracy in the upper limbs with increased trajectory variability in elderly subjects aged 68 to 95 for arm movements during the acceleration and deceleration phases of movement. These changes were attributed to altered motor neuron population or abnormal control of antagonist muscle activity.
<ce:cross-ref refid="bib11">
<ce:sup>11</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>Sensory examination of the elderly often reveals impairment in primary sensory modalities, such as vibration and proprioception, stereognosis, and two-point discrimination.
<ce:cross-refs refid="bib8 bib30 bib52 bib57 bib81">
<ce:sup>8,30,52,57,81</ce:sup>
</ce:cross-refs>
Potvin et al have reported a 64%, 86%, and 97% decline in vibratory sensation at the wrist, ankle, and great toe, respectively, when comparing elderly subjects with young controls.
<ce:cross-ref refid="bib57">
<ce:sup>57</ce:sup>
</ce:cross-ref>
Cole evaluated tests of two–point discrimination which revealed an inability of elderly subjects (ages 71–92 years) to perceive two points at separation distances less than 2.0 mm, whereas none of the control group (ages 17–32 years) required distances of separation greater than 2.0 mm.
<ce:cross-ref refid="bib8">
<ce:sup>8</ce:sup>
</ce:cross-ref>
Grip forces in the elderly group were, on average, over twice as large as the control group, suggesting that impaired sensory discrimination may lead to increased grip forces and limited dexterity.
<ce:cross-ref refid="bib8">
<ce:sup>8</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>Balance and postural control are accomplished through the integration of intact somatosensory systems, vestibular input, central postural reflexes, and motor output. Sensory ataxia results from decline in proprioception and vibratory sensation, frequently observed in the elderly. Vestibular and visual function are special senses necessary for postural control that also decline with age.
<ce:cross-refs refid="bib45 bib54">
<ce:sup>45,54</ce:sup>
</ce:cross-refs>
Under test conditions where somatosensory input is limited, older persons lose their balance much more frequently than younger persons.
<ce:cross-refs refid="bib15 bib43 bib84">
<ce:sup>15,43,84</ce:sup>
</ce:cross-refs>
</ce:para>
<ce:para>Sway results from alternating agonist and antagonist muscle activity in the legs and trunk and is required for maintenance of upright stance. Although changes in the activity of these muscles are usually imperceptible, sway is exaggerated in the normal elderly person, resulting in postural instability.
<ce:cross-refs refid="bib43 bib53 bib84">
<ce:sup>43,53,84</ce:sup>
</ce:cross-refs>
Studies have suggested the elderly have disordered coordination of postural reflexes with voluntary sway.
<ce:cross-refs refid="bib15 bib74 bib85">
<ce:sup>15,74,85</ce:sup>
</ce:cross-refs>
Stelmach et al studied age–related changes in functional relationships between postural reflexes and voluntary movement through electromyography and found that older adults (ages 61–78) had slower, less reliable postural reflexes that were less responsive to the demands of voluntary movement.
<ce:cross-ref refid="bib74">
<ce:sup>74</ce:sup>
</ce:cross-ref>
These investigators also found that functional muscles were less likely to be activated at the same time on the right and left sides, and older adults displayed less inhibition of inappropriate muscle activity.
<ce:cross-ref refid="bib74">
<ce:sup>74</ce:sup>
</ce:cross-ref>
To complicate this picture, anteroposterior displacement, a measure of the functional base of support, decreases by about 33% from the third to the eighth decades;
<ce:cross-ref refid="bib31">
<ce:sup>31</ce:sup>
</ce:cross-ref>
and is further reduced in patients with PD.
<ce:cross-ref refid="bib66">
<ce:sup>66</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>Ambulation requires integration of intact sensory, motor, cerebellar, and higher cortical pathways. Differentiation between gait disorders caused by disease and gait changes related to age is important, as a treatable cause may be found in approximately 25% of cases.
<ce:cross-ref refid="bib75">
<ce:sup>75</ce:sup>
</ce:cross-ref>
The diagnosis of treatable causes is made possible through detailed musculoskeletal, sensory, motor, and reflex examinations. One community study revealed musculoskeletal causes as more common than neurologic causes of gait impairment in the elderly,
<ce:cross-ref refid="bib42">
<ce:sup>42</ce:sup>
</ce:cross-ref>
and skeletal surveys reveal evidence of osteoarthritis in up to 85% of the population beyond 74 years.
<ce:cross-ref refid="bib50">
<ce:sup>50</ce:sup>
</ce:cross-ref>
Age–related factors contributing to impaired ambulation include decreased speed and stride length and one common denominators in gait disturbances of various neurologic etiologies.
<ce:cross-ref refid="bib15">
<ce:sup>15</ce:sup>
</ce:cross-ref>
Some investigators suggest these changes to be a function of increased joint stiffness, decreased proximal muscle strength, energy conservation strategies, or increased “double support time,” defined as the amount of time during a stride when both feet have contact with the ground, which can serve to improve balance.
<ce:cross-refs refid="bib1 bib14 bib15 bib75">
<ce:sup>1,14,15,75</ce:sup>
</ce:cross-refs>
Speed decline is approximately 1.6% per year after age 63 in subjects free of orthopedic, cardiopulmonary, neurologic, or cognitive problems.
<ce:cross-ref refid="bib22">
<ce:sup>22</ce:sup>
</ce:cross-ref>
Walking speed is a crucial factor in crossing intersections safely. Howie and Rubinstein found that 27% of 592 older adult pedestrians were unable to reach the opposite curb in the usual amount of time allowed for pedestrians crossing an intersection.
<ce:cross-ref refid="bib25">
<ce:sup>25</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>Senile gait disorder is traditionally described as a gait disorder associated with aging, unrelated to systemic or neurologic disease, but some have suggested that senile gait disorder might represent the preclinical phase of a slowly evolving neurologic disorder. A number of reports have linked cognitive decline,
<ce:cross-ref refid="bib86">
<ce:sup>86</ce:sup>
</ce:cross-ref>
extra-pyramidal dysfunction,
<ce:cross-ref refid="bib9">
<ce:sup>9</ce:sup>
</ce:cross-ref>
musculoskeletal abnormalities,
<ce:cross-ref refid="bib73">
<ce:sup>73</ce:sup>
</ce:cross-ref>
or ventriculomegaly
<ce:cross-ref refid="bib37">
<ce:sup>37</ce:sup>
</ce:cross-ref>
to this condition. Clinically, senile gait disorder is characterized by the gradual development of a broad-based gait with small steps, diminished arm swing, stooped posture, flexion at hips and knees, difficulty with turning and initiating steps, or tendency toward falling.
<ce:cross-ref refid="bib9">
<ce:sup>9</ce:sup>
</ce:cross-ref>
Patients with senile gait disorder walk less than half as fast as healthy older adults, with shorter stride lengths, an increased percent of stride in double support, and abnormal foot-floor contact and clearance.
<ce:cross-ref refid="bib6">
<ce:sup>6</ce:sup>
</ce:cross-ref>
Although gait impairment is common in the elderly, it should be emphasized that it is not an inevitable result of aging,
<ce:cross-ref refid="bib6">
<ce:sup>6</ce:sup>
</ce:cross-ref>
and it has been repeatedly demonstrated that exercise or an active lifestyle can result in significant gait improvement.
<ce:cross-refs refid="bib3 bib16 bib23 bib44 bib65 bib86">
<ce:sup>3,16,23,44,65,86</ce:sup>
</ce:cross-refs>
</ce:para>
</ce:section>
<ce:section id="cesec3">
<ce:section-title>Hypokinetic Movement Disorders and Normal Aging</ce:section-title>
<ce:para>PD affects approximately 1% of the general population over 60 years of age, and 1.5 million Americans. Although some signs of PD, such as bradykinesia, rigidity, and postural instability, may be seen with normal aging, the degree of impairment is much greater in PD patients. Other factors that differentiate normal aging from PD include absence of rest tremor, symmetric neurologic findings, and lack of response to dopaminergic therapy.
<ce:cross-refs refid="bib51 bib55 bib61">
<ce:sup>51,55,61</ce:sup>
</ce:cross-refs>
</ce:para>
<ce:para>In an effort to estimate the prevalence of parkinsonian signs in the elderly, Bennett et al studied 467 normal elderly residents over the age of 65 in a Boston community by structured neurologic examination.
<ce:cross-ref refid="bib4">
<ce:sup>4</ce:sup>
</ce:cross-ref>
The study revealed several age-specific trends for bradykinesia, rigidity, and gait disturbance. The prevalence of bradykinesia, represented in this study by paucity of movements of the face and extremities and slow finger taps, was estimated at 30.1% for individuals aged 85 and older. Lower extremity rigidity was present in 43.3%–46.3% of individuals over age 85. Gait disturbance, reflected by reduced arm swing, shuffling gait, and prolonged turning, also increased with age. Shuffling gait was observed in 6.4% of individuals in the 65–74 age group, and 29.7% of individuals in the 85 and older age group. Furthermore, the presence of two or more of these categories—criteria used in the diagnosis of early PD—also increased with age: 14.9% in the 65 to 74 age group, 29.5% in the 75 to 84 age group, and 52.4% in the age group over 85.
<ce:cross-ref refid="bib4">
<ce:sup>4</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>Age has been described as a significant risk factor in the development of parkinsonian signs, and age may also have a significant influence on the course of PD. PD is primarily a disease of older individuals, with the mean age of onset in the seventh decade, although rarely it may begin during the third or fourth decade of life.
<ce:cross-ref refid="bib68">
<ce:sup>68</ce:sup>
</ce:cross-ref>
Zetusky et al noted that patients with tremor had an earlier age of onset and a more benign course.
<ce:cross-ref refid="bib87">
<ce:sup>87</ce:sup>
</ce:cross-ref>
Earlier age of onset is more often associated with motor fluctuations and dystonia, and later age of onset of PD correlates with gait disturbance, postural instability, dementia, and increased susceptibility to adverse effects of PD medications.
<ce:cross-refs refid="bib19 bib39 bib68 bib87">
<ce:sup>19,39,68,87</ce:sup>
</ce:cross-refs>
</ce:para>
</ce:section>
<ce:section id="cesec4">
<ce:section-title>Hyperkinetic Movement Disorders in Normal Aging</ce:section-title>
<ce:para>Hyperkinetic disorders include tremor, chorea, myoclonus, tics and stereotypies. Tremor is defined as a regular, rhythmical oscillatory movement resulting from alternating contraction of agonist and antagonist muscle groups. Essential tremor (ET) is estimated to affect five million individuals in the United States, and increases dramatically with age.
<ce:cross-refs refid="bib34 bib61">
<ce:sup>34,61</ce:sup>
</ce:cross-refs>
Rajput et al retrospectively studied ET in Rochester, Minnesota and found the following age–specific annual incidence rates per 100,000: 72.6 between the ages of 60 and 69, 105.8 between the ages of 70 and 79, and 135.7 in those over 80 years of age.
<ce:cross-ref refid="bib60">
<ce:sup>60</ce:sup>
</ce:cross-ref>
Prevalence rates of ET were studied in a Finnish population, and rates increased from 6.84% in ages 60–69, to 12.6% in ages 70–79.
<ce:cross-ref refid="bib62">
<ce:sup>62</ce:sup>
</ce:cross-ref>
Although essential tremor is commonly mistaken as a feature of “old age,” a strong family history and more recently identified genetic markers suggest that ET has a genetic basis and is not simply the product of normal aging.
<ce:cross-ref refid="bib34">
<ce:sup>34</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>Several effects of aging have been identified in patients with ET, most notably a slow progression over many years, with an increase in amplitude or a spread to involve other body parts than those involved at the onset of tremor.
<ce:cross-ref refid="bib36">
<ce:sup>36</ce:sup>
</ce:cross-ref>
Others report lower–frequency tremor, less hand involvement and less associated dystonia in older subjects compared with younger subjects,
<ce:cross-ref refid="bib41">
<ce:sup>41</ce:sup>
</ce:cross-ref>
and increased difficulty with tandem walking.
<ce:cross-ref refid="bib26">
<ce:sup>26</ce:sup>
</ce:cross-ref>
Jankovic et al studied the longevity and frequency of familial tremor in relatives of patients with ET, PD, and healthy controls, and found that parents with tremor lived 9.2 years on average longer than those without tremor.
<ce:cross-ref refid="bib28">
<ce:sup>28</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>Chorea is an irregular, rapid series of movements that flow from one body part to another, without a predictable pattern, and is most often seen in patients with Huntington's disease (HD). Senile chorea is rare and slowly progressive, with generalized symmetric choreiform movements usually beginning in the face or upper limbs, in the absence of other movement disorders, dementia, family history, or neuroleptic exposure. Senile chorea and sporadic, late–onset Huntington's disease (HD) may be clinically indistinguishable. One prospective multicenter study revealed a diagnosis of sporadic, late–onset HD in three of six patients who met clinical criteria for senile chorea; in these patients, abnormal expansions of CAG repeats (IT15) on chromosome 4 were in the lower limits of abnormality (38–40 triplets), perhaps explaining the mild clinical symptoms in these patients.
<ce:cross-ref refid="bib18">
<ce:sup>18</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>Tardive dyskinesia represents a wide variety of involuntary movement, including chorea, dystonia, akathisia, stereotypies, myoclonus and tremor, that result from exposure to dopamine receptor blocking agents, such as phenothiazines or anti-emetic drugs.
<ce:cross-ref refid="bib71">
<ce:sup>71</ce:sup>
</ce:cross-ref>
The overall prevalence rate of tardive dyskinesia among individuals exposed to these agents is approximately 13.9 %.
<ce:cross-ref refid="bib21">
<ce:sup>21</ce:sup>
</ce:cross-ref>
There are reports that 64% of psychiatric patients over the age of 70, compared with 14.8% of patients in the third to fifth decades of life are affected.
<ce:cross-ref refid="bib69">
<ce:sup>69</ce:sup>
</ce:cross-ref>
Loss of D
<ce:inf>2</ce:inf>
receptors in the neostriatum has been associated with this iatrogenic movement disorder,
<ce:cross-ref refid="bib13">
<ce:sup>13</ce:sup>
</ce:cross-ref>
although little is known about the exact pathophysiology.</ce:para>
<ce:para>The most common manifestation of tardive dyskinesia is stereotypy, or rhythmic involuntary movements.
<ce:cross-ref refid="bib70">
<ce:sup>70</ce:sup>
</ce:cross-ref>
In a review of 100 consecutive patients with tardive dyskinesia, Stacy et al found that 78% of patients manifested stereotypies, with 61 patients demonstrating “classic” orofacial movements.
<ce:cross-ref refid="bib70">
<ce:sup>70</ce:sup>
</ce:cross-ref>
These orofacial stereotypies are indistinguishable from spontaneous oral–lingual–buccal dyskinesias, which occur in the absence of exposure to neuroleptics.
<ce:cross-ref refid="bib83">
<ce:sup>83</ce:sup>
</ce:cross-ref>
Klawans and Barr studied the incidence of spontaneous lingual–facial–buccal dyskinesias and found a 6.8% overall incidence between the ages of 60 and 79; this incidence, similar to tardive dyskinesia, increases with age.
<ce:cross-ref refid="bib33">
<ce:sup>33</ce:sup>
</ce:cross-ref>
Koller studied 75 consecutive edentulous patients, not previously exposed to neuroleptics, in a Veterans Administration dental clinic, and found that 16% of edentulous patients had orofacial dyskinesia.
<ce:cross-ref refid="bib38">
<ce:sup>38</ce:sup>
</ce:cross-ref>
Ill fitting or no dentures, were thought to be a risk factor for patients with orofacial dyskinesias.
<ce:cross-ref refid="bib38">
<ce:sup>38</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>The similarities between spontaneous choreiform movements of senile chorea and tardive stereotypy suggest exposure to dopamine receptor blocking agents may hasten the “release” of primitive motor circuits with advancing age. Primitive reflexes, or “release” phenomena, resulting from impaired cerebral inhibition of lower centers, are common in neurodegenerative disorders.
<ce:cross-ref refid="bib61">
<ce:sup>61</ce:sup>
</ce:cross-ref>
Moreover, several studies have revealed increased primitive reflexes, such as snout, grasp, and palmomental reflexes, in the normal elderly population.
<ce:cross-refs refid="bib27 bib30 bib52">
<ce:sup>27,30,52</ce:sup>
</ce:cross-refs>
Prevalence rates in one study for the snout reflex were 33% in the 65–74 age group, compared with 73% in the 85+ age group; prevalence rates for the grasp reflex were 27% in the 65–74 age group, compared with 67% in the 85+ age group.
<ce:cross-ref refid="bib52">
<ce:sup>52</ce:sup>
</ce:cross-ref>
The incidence of the palmomental reflex in another study was 20% in the fifth decade compared with 60% in the ninth decade.
<ce:cross-ref refid="bib27">
<ce:sup>27</ce:sup>
</ce:cross-ref>
</ce:para>
<ce:para>Other hyperkinetic disorders that occur with increased frequency in the elderly population include dystonia, hemiballismus, myoclonus, and periodic limb movements of sleep. Most adult-onset focal dystonias have onset in the fourth to sixth decades; the onset of blepharospasm is generally in the sixth decade.
<ce:cross-ref refid="bib77">
<ce:sup>77</ce:sup>
</ce:cross-ref>
Hemiballismus most often occurs in the setting of stroke, which is a common disorder of aging.
<ce:cross-ref refid="bib61">
<ce:sup>61</ce:sup>
</ce:cross-ref>
Myoclonus may occur in the setting of metabolic derangements and certain neurodegenerative disorders that have increased frequency with age, such as Alzheimer's disease, Creuzfeldt–Jakob disease, or corticobasal degeneration.
<ce:cross-ref refid="bib61">
<ce:sup>61</ce:sup>
</ce:cross-ref>
High prevalence rates for periodic leg movements of sleep (PLMS) are seen in the general population over the age of 65. In one community study, 427 individuals, ages 65 and over, were evaluated for signs of PLMS, with 45% demonstrating highly suggestive symptoms.</ce:para>
</ce:section>
<ce:section id="cesec5">
<ce:section-title>Summary</ce:section-title>
<ce:para>Normal aging is associated with a variety of changes in the nervous system, many of which manifest as motor impairment. While every effort should be made to determine possible treatable causes for motor decline or involuntary movements in the normal elderly individual, treatment most often will be of a conservative nature, and should include physical therapy or occupational therapy. It should be emphasized that significant neurologic deterioration is not an inevitable aspect of aging. Recent articles and studies have focused on differentiating “successful” aging from “usual”aging.
<ce:cross-refs refid="bib30 bib52 bib64">
<ce:sup>30,52,64</ce:sup>
</ce:cross-refs>
The challenge for future studies will be to determine those factors that lead to successful aging, thereby allowing clinicians to educate patients on how to achieve optimal health in their later years.</ce:para>
</ce:section>
</ce:sections>
</body>
<tail>
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