Clorazepate chemical structure
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Tranxene

Clorazepate (brand name: Tranxene®) is a member of the group of drugs called benzodiazepines. Benzodiazepines are prescribed by general practitioners and psychiatrists in the treatment of anxiety disorders and insomnia. They may also be prescribed as anticonvulsants and muscle relaxants. In the twenty-first century, clorazepate is principally prescribed in the treatment of alcohol withdrawal and epilepsy, though of course it is a useful anxiolytic because of its long half-life. The normal starting dosage range of clorazepate is 15-60 mg 2-4 x per day. Dosages as high as 90-120 mg per day may be used in the treatment of acute alcohol withdrawal. Clorazepate is available in 3.75, 7.5, and 15 mg capsules or tablets. more...

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Clorazepate SD (controlled release) is available in 11.25 and 22.5 mg tablets. Clorazepate SD is only prescribed when the patient has become adjusted to a certain dosage, and is taken once a day. Clorazepate is available in generic form. Clorazepate begins to act on the central nervous system within one or two hours, and its effects may be felt for an entire day or longer in some individuals. It is contraindicated for those with impaired renal or hepatic function. Clorazepate is listed under Schedule IV of the Controlled Substances Act and is as highly addictive as the other benzodiazepines. Clorazepate was approved for use in the United States by the Food and Drug Administration in 1972.

Interactions

All sedatives are likely to magnify the effects of Tranxene on the central nervous system. Cimetidine inhibits breakdown of clorazepate, and leads to increased levels of the drug in the system.

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Trunk muscle performance in early parkinson's disease
From Physical Therapy, 6/1/98 by Bridgewater, Karen J

Background and Purpose. Altered trunk function has been observed in people with Parkinson's disease (PD). Subjects. This study investigated the trunk function of people with PD, as compared with people without PD. Methods. Range of motion (against 1 Nm of resistance), isometric torque, and isoinertial performance against moderate resistance were assessed using an Isostation B-200. Results. Group effects between the subjects with PD and the subjects without PD were found for all variables. Range of motion into extension and maximum and average isometric torque in the directions of extension and right rotation showed group effects between subjects classified as being in Hoehn and Yahr stage I and subjects classified as being in Hoehn and Yahr stage II. Conclusion and Discussion. People with PD exhibit less axial range of motion and isometric and isoinertial ability compared with persons without PD. There is a loss of the ability to extend the trunk early in the disease. These findings suggest the importance of further investigation into the role of strengthening programs soon after a diagnosis of PD in order to potentially delay changes in trunk function and subsequent functional difficulties. [Bridgewater KJ, Sharpe MH. Trunk muscle performance in early Parkinson's disease. Phys Ther. 1998;78:566-576.]

Key Words: Muscle performance, trunk; Neck and trunk, general; Neuromuscluer disorders, Parkinson's disease.

Parkinson's disease (PD) is a chronic, progressive disease of the nervous system. The three primary symptoms of PD are tremor, bradykinesia, and rigidity, but other signs and symptoms, such as muscle stiffness and weakness,l2 are frequent complaints associated with PD. James Parkinson not only alluded to the presence of weakness in the title of his 1817 publication, An Essay on the Shaking Palsy,3 but he also wrote in the text of "lessened muscular power." Although people with PD often complain of difficulty with the development of muscle power,1 detectable weakness during manual muscle testing is characteristically absent.24 Even with the use of quantitative techniques of measuring muscle torque, results are conflicting. Researchers have supported4-7 and disputedl2 the presence of deficits in torque production. Methodological differences between, or even within, studies and possibly the wide range of forces their subjects develop are likely to be common sources of discrepant results. Several studies have investigated maximum isometric torque production,'s7 a task that, in our opinion, does not involve the confounding factors of visual perception, estimation, prediction, and spatial orientation. Alternatively, isotonic performances (ie, motor function involving moving a set weight through a given range) also have been considered.2 Nevertheless, questions remain as to the presence and nature of weakness during functional activities (functional weakness) in persons with PD.

Two groups of researchers have demonstrated the effect of PD on muscle performance by examining the effect of pharmacological treatment on torque developed during isokinetic movements7 and isometric6.7 torque production. Corcos et al6 hypothesized that if patients were weaker when not receiving medication, the difference in performance could be attributed to the effect of PD. Both groups found that selected variables decreased in torque production after withdrawal of medication (that is, Pedersen and Oberg7 found decreased torque production at almost all speeds, and Corcos et al6 found isometric elbow extension torque production to be affected). Pedersen and Oberg proposed that alterations to muscle performance may be subtle, although meaningful, and that sensitive dynamometric assessment could identify impairments otherwise undetected by traditional manual muscle testing.

Evidence indicates that central mechanisms may be responsible for muscle weakness in people with PD.46 In a group of subjects with PD, Yanagawa and associates4 compared the maximum isometric torque produced during voluntary ankle dorsiflexion with the torque produced by tetanic contraction of pretibial muscles by repetitive electrical stimulation of the common peroneal nerve. They also compared the performance of the subjects with PD with that of age- and sex-matched subjects who were neurologically intact. The researchers found the voluntary force of isometric ankle dorsiflexion to be reduced in the subjects with PD. There was no difference in performance, however, between the subjects with PD and the subjects without PD when force was produced by electrical stimulation. They also found no relationship between voluntary torque and rigidity, tremor, or Hoehn and Yahr classification of the patients' status. Because the voluntary isometric torque in the subjects with PD was less than that in subjects without PD, yet the torque provoked by tetanic stimulation did not differ, changes in tissue leading to increased stiffness seem unlikely to influence muscle torque generation in people with PD.4 Furthermore, because antiparkinsonian medication is not known to affect peripheral neuromuscular function, the differences in force between subjects who were on and off medications support the hypothesis that the source of weakness in persons with PD is primarily central in origin.6

Diminished voluntary muscle force in persons with PD may be a response to a decrease in tonic activity of the agonist muscle6 rather than to the mechanisms associated with rigidity, tremor, or the slow development of muscle power,4 although the rate of force development has been shown to be deficient.589 Furthermore, the selective effects of central deficits, through neuroanatomical connections with particular spinal pathways, may explain the decreased maximum force production of more proximal muscle groups, with absence of grip torque production deficit.iQ. Irrespective of the underlying neurological phenomena, it is likely that persons with PD are less capable of generating maximum force than are elderly persons without disease and that this deficit may cause functional difficulties and a perception of weakness.

Persons with hemiparkinsonism showed no deficit in isometric grip force according to Koller and Kase.2 The same subjects, however, exhibited deficits in torque production bilaterally, as measured by a repetitive isotonic motor test2 involving moving a set weight through a given range. Torque generation (in foot-pounds) in flexion and extension at the wrist, arm, and knee (as measured by the Cybex II isokinetic dynamometer*) over the second, third, and fourth repetitions was reduced in the subjects with PD as compared with the subjects without PD.2 The decrease in torque development did not correlate with any particular symptom (tremor or rigidity), implying that a mechanism other than that related to the classic symptoms of PD may be responsible for the torque production deficit. Koller and Kase2 proposed that the slightly greater weakness associated with the affected side may represent the added decline in motor performance resulting from tremor or rigidity.

Power depends on movement speed, which may be reduced by mechanisms other than the rate of muscle fiber contraction, such as slow recruitment of motor units, rigidity in antagonists, or bradykinesia.4 Hypotheses regarding such factors would also support the observed decreases in the rate of isometric force generation.

A number of nervous system deficits associated with PD may contribute to functional weakness. In particular, motor unit discharge, influenced by supraspinal, spinal, and peripheral inputs,?2 is deficient in persons with PD. In addition to an initial delay in motor unit recruitment, PD results in a slowness in motor unit recruitment,l3 motor unit discharge asynchronization, and the occurrence of paired discharges.lY Neuromuscular changes, therefore, can render the person with PD disadvantaged in attempts to recruit units to adequate force levels and to sustain or modulate motor responses.

Despite the clinical observations of trunk involvement and postural changes in persons with PD,14.15 no studies have investigated trunk muscle performance in people with PD. Abnormalities of trunk muscle function may be present clinically as difficulty in walking and turning, a tendency to fall, and difficulty in turning or inability to turn in bed. The obvious, yet gradual, change in posture toward flexion can be accompanied by weakness of the back extensors and spinal stiffness with or without associated pain. Respiration is also threatened by the large changes in trunk posture, an important phenomenon given the threat of pneumonia to the person with PD.ls

The purpose of our study was to compare the trunk muscle performance of a defined group of people with early PD and a group of sex- and age-matched people without known neurological impairment, using the Isostation B-200 triaxial dynamometers to measure trunk function.

Method

Subjects

Thirteen subjects with early PD (Hoehn and Yahr stage I or II, as assessed by a neurologist) and 13 sex- and age-matched subjects with no known neurological impairment participated in the study. All subjects gave written informed consent. Two assessments were conducted, separated by an interval of 14 to 21 days. One subject with PD was unable to successfully complete the initial assessment due to feeling faint. Another subject with PD required hospitalization for a separate medical condition between the first and second assessments. The 11 remaining subjects with PD and the 13 subjects without PD are described in Tables 1 and 2. Apart from 3 subjects with ischemic heart disease, arthritis, and osteoporosis, respectively, the medical histories of the subjects without PD were unremarkable. Among the subjects in this group, subject 1 was taking Betaloc and aspirin; subject 2 was taking Premarin; subject 3 was taking Capoten; subject 5 was taking Lasix, Midamor, Sultrin, Sinequan, and Tranxene; and subject 9 was taking aspirin.

The subjects with PD were asked to identify what time of day they felt that their medication was most effective. Each individual's assessment was then timed accordingly to occur during the period in which the subject believed there was the greatest medication effect. Each subject was guided by a physical therapist through the 2 assessment sessions. The instructions and order of testing remained constant across all sessions and subjects.

Trunk Assessment

Trunk muscle performance was measured using the Isostation B-200 triaxial dynamometer (Figure). Each subject was asked to lie prone on a treatment couch while three locations were marked on the skin with a pen: (1) the lumbosacral junction, (2) the T12 spinous process, and (3) a distance 2 finger widths (index and middle fingers of the examiner) caudal to the T12 spinous process. These landmarks were used for subject placement in the Isostation B200. Subjects were tested with bare feet. Once strapped into the machine, markers and rulers mounted on the machine by the manufacturer were used for subject placement within the machine. For each subject, the machine setting remained constant across assessments. The order of testing remained constant across all assessments and between all subjects. During each assessment, there was a 2-minute rest period between the 3 main testing procedures (range of motion [ROM], isometric, and resisted isoinertial [movement against a preselected resistance]). During the rest period, the leg straps were released and subjects were requested to gently move their legs until the next test began. In addition to allowing the subjects to rest, we believe that these 2-minute periods also facilitated the action of the venous pump and thus minimized the risk of adverse effects of postural hypotension. Assessment timing is documented in Table 3. During trials, subjects were instructed to either clasp their hands or hold their hands in front of their abdomen (in the epigastric area).

Test-Retest Reliability

Because we believe that the performance of persons with impairments is potentially more erratic than that of persons without impairments and because we wanted to determine the reliability of the testing procedure (not subject reliability), we examined data from the performance of the 13 subjects without PD to determine test-retest reliability. Therefore, we cannot account for the reliability of measurements obtained for our subjects with PD. In accordance with the procedure described by Shrout and Fleiss,'7 test-retest reliability was examined using intraclass correlation coefficients (2,1). The results of sessions 1 and 2 were examined for correlation. Only those measurements that, with the subjects without PD, showed an acceptable level ( >.7) of reproducibility were retained for subsequent examination of the difference in performance between the 2 groups.

The correlation coefficients for test-retest reproducibility of performance variables are reported in Table 4. Range of motion (against 1 Nm of resistance) was more reproducible in the sagittal plane than in the transverse plane. Alternatively, both maximum and average isometric torque readings were highly reproducible in both planes. During isoinertial performance against 50% resistance, velocity measures were generally more reproducible than ROM measures (against the same resistance), with the exception of ROM to the left side. Work and power measures were also highly repeatable. As test-retest reliability was thereby established, data obtained from the first and second assessments were combined into one data set for the analysis of covariance (ANCOVA) examining a group difference between the subjects with PD and the subjects without PD.

Range of Motion

Range of motion was assessed against 1 Nm of resistance with all axes unlocked, allowing freedom of movement in all planes simultaneously. Subjects were instructed to move as far as they could in a slow and controlled manner. The movement pattern of neutral to full flexion, to full extension, and returning to neutral was examined first. This examination was followed by examination of the movement pattern of neutral to full right rotation, to full left rotation, and returning to neutral. Two assessment trials of each movement pattern were performed, with a 1-minute break between trials. A practice trial of each movement pattern was conducted 15 seconds prior to the first assessment trial.

Isometric Performance

During isometric tests (in the order of flexion, extension, right rotation, and left rotation), all axes of the Isostation B-200 were locked mechanically in the neutral upright position, with maximum resistance also applied by the computer software. Subjects were instructed to increase pressure against the machine immediately on hearing the examiner say "go" and to sustain the pressure until they heard the examiner say "stop." Subjects were instructed to produce the pressure against the machine as rapidly as possible, but they were warned against sudden exertion. Each assessment trial contraction lasted 6 seconds and was repeated once after a 60-second rest, thus creating 2 assessment trials. A practice (submaximal) trial in the appropriate direction was performed 15 seconds prior to the first assessment trial in that direction.

Resisted Isoinertial Performance Isoinertial assessment requires the subject to move against a preselected resistance, which, according to the manufacturer of the Isostation 200, remains constant throughout the entire range of movement. Resisted isoinertial performance of the movement pattern of repeated full flexion to full extension was examined first. Following 2 submaximal practice repetitions and a 15-second rest period, one 30-second assessment trial of repeated full flexion to full extension was performed. During the assessment trial, each individual worked against a resistance of 50% of his or her maximum isometric torque production ability. Subjects were instructed to move as fast, as hard, and as far as they could, repeating the full movement pattern until they were told to stop. Following a 2-minute rest period, the same practice and examination procedure was followed for right rotation to left rotation.

Data Extraction

Range of motion and isometric performance. For each session, the greatest of the 2 ROM measurements and the largest of the 2 isometric torques were used for analyses. Maximum and average isometric torque production values were taken from the 5-second period immediately following initiation of isometric torque development during assessment trials, according to the model of Parnianpour et al.'8

Resisted isoinertial performance. Resisted isoinertial performance was quantified by examining repetitions 2, 3, and 4 of the 30-second assessment trial of repeated resisted isoinertial movements in the planes of flexion/ extension and right rotation/left rotation. Values were obtained for maximum and average velocities, power and work done, and total ROM in the primary plane of motion.

During the preliminary analyses, using the Minitab (version 8.2) statistical software package+ and ANCOVAs, the effects of independent variables were considered. All linear independent variables (eg, height, body mass index, age) were placed in an ANCOVA (GLM model) equation as covariates. For the ANCOVA of each dependent variable, through a process of stepwise backward elimination, variables that were not significant (P>.05 and F

When all remaining variables had an F value greater than 1.00, the investigatory process was considered complete and the next dependent variable was examined. The residual models of the 4 ROM variables were then examined to investigate the consistency of independent variables. We wanted to determine, for example, whether any given independent variable was not significant yet another variable was always significant and whether there was a variable that was consistently removed within the first 3 stepwise backward elimination processes. Variables that were not significant in any of the residual models of the 4 ROM variables were excluded from the initial equation for the final analyses. Variables that were significant and present in the residual model on more than one occasion were always retained. The residual models of the group of 4 maximal isometric performances were then considered, followed by those of the resisted isoinertial performances. Ultimately, subjects' ages and sex were included in the analyses as covariates. All dependent variables were examined by ANCOVA (GLM model), using Minitab statistical software. Each dependent variable was considered in turn and the effect of group (PD or normal) was examined (included as a covariate).

Results

Range of Motion (Against IFm of Resistance) For all ROM variables (flexion, extension, right rotation, and left rotation), group effects were found (Tab. 5). Maximal Voluntary Isometric Contraction Group effects were found for all isometric variables (maximum and average flexion, extension, right rotation, and left rotation) (Tab. 6).

Resisted Isoinertial Performance

A group effect was present for all resisted isoinertial variables (ROM and maximum velocity in all 4 directions: average flexion/extension and rotation velocity, flexion/extension and rotation work and power) (Tab. 7).

Hoehn and Yahr Stage

Following the primary analyses, the subjects with PD were further examined to determine whether differences in performance existed between subjects classified as being in Hoehn and Yahr stage I and subjects classified as being in Hoehn and Yahr stage II. Range of motion in extension and maximum and average isometric torque production in extension and right rotation were the only variables that showed a group effect (Tab. 8). Examination of all of the resisted isoinertial variables failed to show the presence of a group effect between subjects classified as being in Hoehn and Yahr stage I and subjects classified as being in Hoehn and Yahr stage II.

Discussion and Conclusion

Our main finding was that the subjects with PD exhibited deficits in both axial torque production and available ROM in the directions of flexion, extension, left rotation, and right rotation. Many clinicians have suspected that trunk muscle weakness is associated with PD, and our study documented the substantial difference in trunk muscle performance between people with PD and people without PD.

It is widely accepted that people with PD have less difficulty with motor function in response to external sensory stimuli than with internally generated or selfinitiated movements.l's-21 Verbal cues of examiners during muscle testing provide an additional auditory stimulus that could assist people with PD in force generation. Because such additional stimuli are not present during an individual's daily life, the weakness may be more pronounced during functional activities. Verbal cues, therefore, may be a confounding variable, with the potential to cause discrepancies between patient reports of weakness and the results of manual muscle testing. Although such verbal cues were present during testing in our study, a deficit in torque production remained evident, implying a weakness of such an extent that it could not be compensated for by auditory stimulation or central activation.

Some authorsl propose that it is the rate of muscle torque development that may be deficient, as opposed to the maximum torque production, which causes people with PD to feel muscular weakness. Manual muscle testing is not designed to measure "tardiness" of torque production, and, given time, the person with PD may be able to achieve a level of force perceived by the examiner as "normal." Studiesl5,6,8,9 examining the rate of force generation are in agreement; the average time taken to reach target forces has been shown to be longer in people with PD. Jordan and associates' found no difference in maximal isometric grip torque development between subjects with PD and subjects without PD, although the rate of force generation was slower among the subjects with PD. This result is supported by studies of isometric elbow flexion.919 In contrast to many studies but supported by the results of a study by Corcos et al,6 our subjects with PD demonstrated a decrease in maximum torque production capability, leading us to suspect that a theory solely attributing perceived weakness to diminished rate of contraction is incomplete.

By investigating differences in performance between subjects classified as being in Hoehn and Yahr stage I and subjects classified as being in Hoehn and Yahr stage II, we examined changes in trunk function and disease progression. No differences were found at a level of statistical significance for any variables, but this finding may be attributable to the small number of subjects in each group (n=5 and n=6, respectively). Both ROM into extension and extensor isometric torque production, however, revealed a group effect between Hoehn and Yahr stages I and II. This result is in keeping with the observations of Corcos et al,e who found a greater reduction in strength in extension than in flexion in subjects after withdrawal of medications. Both our results and those of Corcos et al suggest that extensor muscles become weaker than flexor muscles as the disease progresses, leading to a tendency to adopt flexion postures.

Verbal encouragement may confound results by facilitating the performance of people with PD, although this did not appear to be the case in our study. Verbal encouragement was provided by Koller and Kase2 during motor tests involving moving a set weight through a given range and by Yanagawa et al4 during an isometric task, but Jordan et all appear to have withheld such encouragement. Surprisingly, therefore, Jordan and associates' subjects showed no deficiency in maximum isometric torque production, yet performance of subjects with PD in the studies where encouragement was provided was less than that of their counterparts without PD. In addition, our subjects with PD showed lesser performance in ROM, isometric, and isokinetic testing as compared with the subjects without PD.

Our results regarding a deficiency of isometric torque production support the hypothesis of Corcos et al6 that people with PD are impaired in their ability to generate peak torque. These results, however, are in contrast to those of Jordan et all and Koller and Kase,2 who found no difference in isometric torque production of distal muscles between subjects with PD and subjects without PD. Koller and Kase2 proposed that as the basal ganglia are primarily involved in the use of some muscles to produce a movement, isometric torque production need not be affected adversely. Jordan et all and Corcos et al,s however, documented changes in latency, rate of generation, and relaxation, indicating that isometric torque production is not spared in the disease process. Jordan et all and Koller and Kase2 studied subjects with early PD. Yanagawa and associates4 studied subjects classified as being in Hoehn and Yahr stages I to IV. Corcos et al6 did not indicate the Hoehn and Yahr stages of their subjects. Yanagawa and associates4 found people with PD to be deficient in performance of maximum isometric ankle dorsiflexion, a result that is consistent with our study. Koller and Kase2 and Yanagawa et al4 studied distal musculature, as opposed to the proximal musculature we examined. Given the premise, supported by findings of animal studies, that proximal musculature is more under the control of the structures affected by PD and may be affected to a greater extent than distal musculature,lo1l the differences in results among reports of isometric performance are interesting. It is possible that axial musculature is affected by weakness in the early stages of the disease. Alternatively, distal musculature may demonstrate only subtle changes in isometric torque production until later in the disease process.

Deficits in muscle performance when moving a set weight through a given range have been addressed to a lesser extent in the literature. As recognized by Jordan et al,l the results of studies examining isometric tasks and the results of studies examining isokinetic tasks should be compared with care because tasks involving movement require movement preparation, distance estimation, spatial orientation, and selection of appropriate forces. Cognitive contributions to task performance, therefore, may be greater with isokinetic testing. Some studies have examined the achievement of submaximal target forces, considering factors such as reaction time or spatial organization of movement." Similarly, such studies, with their cognitive component, should not be compared with studies examining maximum isotonic (moving a set weight through a given range), isoinertial, or isokinetic torque production attempts. People with PD, however, have exhibited isotonic muscular weakness,2.7 a result that is supported by our results regarding resisted isoinertial performance.

Functional weakness, characterized by decreased muscle torque production ability and ROM, may be the result of many coexisting factors. Disrupted motor planning,2 peripheral neuromuscular changes,4 altered characteristics of the noncontractile muscle elements,4 abnormal discharge characteristics of motor units,l2 disuse weakness,22 and muscular rigidity23 have all been considered by researchers in the past. Regardless of the cause, decreased ability to develop torque can result in a perception of weakness for people with PD.

The results of our study emphasize the importance of addressing altered trunk muscle function in patients from the time of diagnosis of their PD. A deficiency in trunk muscle performance has been shown to occur in the very early stages of the disease, particularly in the trunk extensors and rotators.

Further research is needed to investigate whether relationships exist between trunk muscle performance and function and to develop treatment regimens that could minimize the effect of the disease process on trunk muscle performance, thereby delaying or preventing associated disability and maximizing the quality of life of persons with PD.

-ma 1

t Isotechnologies Inc, PO Box 1239, Hillsborough, NC 27278.

Minitab Inc, 3081 Enterprise Dr, State (ollege, PA 16801-3008.

References

1 Jordan N, Sagar HJ, Cooper JA. A component analysis of the generation and release of isometric force in Parkinson's disease. J Neurol Neurosurg Psychiatry. 1992;55:572-576. 2 Koller W, Kase S. Muscle strength testing in Parkinson's disease. Eur Neurol. 1986;25:130-133.

3 Parkinson J. An Essay on the Shaking Palsy. London, England: Sherwood, Nesly and Jones; 1817.

4 Yanagawa S, Shindo M, Yanagisawa N. Muscular weakness in Parkinson's disease. Adv Neurol. 1990;53:259-269. 5 Stelmach GE, Worringham CJ. The preparation and production of isometric force in Parkinson's disease. Neuropsychologia. 1988;26: 93-103.

6 Corcos DM, Chen C-M, Quinn NP, et al. Strength in Parkinson's disease: relationship to rate of force generation and clinical status. Ann Neurol.1996;39:79-88.

7 Pedersen SW, Oberg B. Dynamic strength in Parkinson's disease: quantitative measurements following withdrawal of medication. Eur Neurol. 1993;33:97-102.

8 Stelmach GE, Teasdale N, Phillips J, Worringham CJ. Force production characteristics in Parkinson's disease. Exp Brain Res. 1989;76: 165-172.

9 Wierzbicka MM, Wiegner AW, Logigian EI., Young RR. Abnormal most-rapid isometric contractions in patients with Parkinson's disease. J Neurol Neurosurg Psychiatry. 1991;54:210-216. 10 Lawrence DG, Kuypers HG. The functional organization of the motor system in the monkey, I: the effects of bilateral pyramidal lesions. Brain. 1968;91:1-14.

11 Lawrence DG, Kuypers HG. The functional organization of the motor system in the monkey, II: the effects of lesions of the descending brain-stem pathways. Brain. 1968;91:15-36.

12 Dengler R, Konstanzer A, Gillespie J, et al. Behavior of motor units in parkinsonism. Adv Neurol. 1990;53:167-173. 13 Rogers MW. Motor control problems in Parkinson's disease. In: Lister MJ, ed. Contempora Management of AMotor Control Problems: Proceedings of the II Step Conference. Alexandria, Va: Foundation for Physical Therapy Inc; 1991.

14 Banks MA. Physiotherapy. In: Caird FI, ed. Rehabilitation in Parkinson's Disease. London, England: Chapman and Hall Ltd; 1991:45-65.

15 Stern G, Lees A. Parkinson's Disease: The Facts. New York, NY: Oxford University Press Inc; 1991.

16 McElvaney NG, Wilcox PG, Chung A. Pleuropulmonary disease during bromocriptine treatment of Parkinson's disease. Arch Intern Med. 1988;148:2231-2236.

17 Shrout PE, Fleiss JL. Intraclass correlations: uses in assessing rater reliability. Psychol Bull. 1979;86:420-428. 18 Parnianpour M, Nordin M, Frankel VH, Kahanovitz N. Triaxial coupled maximal isometric trunk strength measurements. Paper pre

sented at Annual Meeting of the Orthopaedic Research Society, 1988, Atlanta, Ga.

19 Deeke L. Cerebral potentials related to voluntary actions: parkinsonian and normal subjects. In: Delwaide PJ, Agnoli A, eds. Clinical Neurophysiology in Parkinsonism. New York, NY: Elsevier Science Inc; 1985:90-105.

20 Forssberg H, Johnels B, Steg G. Is parkinsonian gait caused by a regression to an immature walking pattern? Adv Neurol. 1984;40: 375-379.

21 Lee RG. Pathophysiology of rigidity and akinesia in Parkinson's disease. Eur Neurol 1989;29(suppl 1):13-18. 22 Schenkman ML, Butler RB. A model for multisystem evaluation and treatment of individuals with Parkinson's disease. Phys Ther. 1989;69: 932-943.

23 Cantello R, Gianelli hZ, Bettucci D, et al. Parkinson's disease rigidity: magnetic motor evoked potentials in a small hand muscle. Neurology. 1991;41:1449-1456.

KJ Bridgewater, PhD, BApplSc(Physio), Hons, is Research Fellow, Motor Control and Motor Learning Laboratory, School of Physiotherapy, University of South Australia, North Terrace, Adelaide, South Australia 5000, Australia (margie.sharpe@unisa.edu.au). Address all correspondence to Dr Bridgewater

MH Sharpe, PhD, Sc, BApplSc(Physio), AUA, is Associate Professor in Neurological Physiotherapy and Head of the Motor Control and Motor Learning Laboratdfl, School of Physiotherapy, University of South Australia.

This study was appoved by the University of South Australia Human Research Ethics Committee.

Copyright American Physical Therapy Association Jun 1998
Provided by ProQuest Information and Learning Company. All rights Reserved

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