Parkinson Disease: Comella CL

Comella CL. · No affiliation provided · JAMA. · Pubmed #11798375 No free full text.

This publication has no abstract.

Weintraub D, Comella CL, Horn S. · Department of Psychiatry and Neurology, University of Pennsylvania, 3615 Chestnut St, Philadelphia, PA 19104, USA. · Am J Manag Care. · Pubmed #18402509 links to  free full text

Abstract: The nonmotor neuropsychiatric symptoms of Parkinson's disease, particularly depression, psychosis, and cognitive impairment/dementia, are major contributors to disability and a decline in quality of life. Their effect on patients may be more disabling than motor symptoms. Increasing awareness of the importance of recognizing and treating neuropsychiatric symptoms of this disease in the medical community is a focus of specialists and organizations. This article looks at useful screening measures to help clinicians recognize neuropsychiatric symptoms and offers suggestions for their effective treatment.

Weintraub D, Comella CL, Horn S. · Department of Neurological Sciences, University of Pennsylvania, 330 S 9th St, Philadelphia, PA 19107, USA. · Am J Manag Care. · Pubmed #18402508 links to  free full text

Abstract: In the absence of a cure, the primary goals in managing Parkinson's disease (PD) are to preserve functionality and health-related quality of life. Meeting these goals can minimize healthcare-resource utilization and long-term healthcare costs. Although effective treatment of motor symptoms of the disease is a central consideration to facilitate improved outcomes, management of nonmotor symptoms is now recognized as an equally important target of intervention, since nonmotor symptoms can contribute greatly to disability. The article addresses the current treatment options of choice for reducing motor symptoms of PD and their most rational use. Cost-effectiveness is a major consideration for managed care and is also analyzed for many available treatment options.

Weintraub D, Comella CL, Horn S. · University of Pennsylvania, Philadelphia, PA, USA. · Am J Manag Care. · Pubmed #18402507 links to  free full text

Abstract: Parkinson's disease (PD) is a chronic neurodegenerative disease associated with substantial morbidity, increased mortality, and high economic burden. Of importance to managed care is that the number of cases of PD are on the rise, paralleling the advancing age of the population, and misdiagnosis is common. Effective management of PD can minimize disability and potentially improve long-term outcomes, which would minimize long-term healthcare costs and medical resource utilization. This article provides a brief review of the epidemiology, pathophysiology, clinical course, and burden of PD.

Comella CL. · Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois 60612, USA. · Mov Disord. · Pubmed #18175398 No free full text.

Abstract: Sleep disturbances are one of the most common of the nonmotor complications of Parkinson's disease (PD), and increase in frequency with advancing disease. The causes of sleep disturbance in PD are numerous, and many patients may have several factors that contribute. These disorders can be broadly categorized into those that involve nocturnal sleep and daytime manifestations such as excessive daytime sleepiness. Some sleep disorders, in particular REM sleep behavior disorder (RBD) and excessive daytime sleepiness (EDS) may arise as a primary manifestation of PD, reflecting the anatomic areas affected by the neurodegenerative process. Appropriate diagnosis of the sleep disturbance affecting a PD patient can lead to specific treatments that can consolidate nocturnal sleep and enhance daytime alertness.

Iranzo A, Comella CL, Santamaria J, Oertel W. · Neurology Service, Hospital Clínic and Institut D'Investigació Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain. · Mov Disord. · Pubmed #17534950 No free full text.

Abstract: The pathophysiology of restless legs syndrome (RLS) is associated with central dopaminergic system dysfunction leading to speculations that RLS may be common in those neurodegenerative diseases with dopaminergic cell loss. However, since RLS is a very common condition, the co-occurrence with less frequent disorders such as the neurodegenerative diseases might be a matter of chance. Currently, no data suggests that patients with sporadic and familial RLS are at increased risk for developing a neurodegenerative disease. In particular, whether RLS is associated with Parkinson's disease has not been established. Only a few studies have directly addressed this issue, and these have methodological limitations yielding conflicting results. Few studies have assessed the frequency of RLS in other neurodegenerative disorders. In several autosomal dominant spinocerebellar ataxias, particularly in Machado-Joseph disease, a higher frequency of RLS is reported than could be accounted for in the general population. Two anecdotal publications have reported the presence of RLS in patients with Huntington's disease and hereditary spastic paraparesis. There are no studies that have examined the association between RLS and other neurodegenerative diseases, such as Alzheimer's disease, frontotemporal dementia, dementia with Lewy bodies, multiple system atrophy, progressive supranuclear palsy, and corticobasal degeneration. .

Comella CL. · Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA. · J Neural Transm Suppl. · Pubmed #17017552 No free full text.

Abstract: Sleep disturbances are frequent in Parkinson disease. These disorders can be broadly categorized into those that involve nocturnal sleep and excessive daytime sleepiness. The disorders that are often observed during the night in PD include sleep fragmentation that may be due to recurrent PD symptoms, sleep apnea, Restless Leg Syndrome/ periodic limb movements and REM sleep behavior disorder. Excessive daytime sleepiness is also a common occurrence in PD. EDS can arise from several etiologies, and patients may have more than one etiology responsible. The causes of EDS include nocturnal sleep disorder with sleep deprivation and resulting daytime somnolence, the effect of drugs used to treat PD, and possibly neurodegeneration of central sleep/wake areas. Appropriate diagnosis of the sleep disturbance affecting a PD patient can lead to specific treatments that can consolidate nocturnal sleep and enhance daytime alertness.

Comella CL. · Department of Neurological Sciences, Rush-Presbyterian-St. Luke's Medical Center, Rush Medical College, 1725 West Harrison, Suite 755, Chicago, IL 60612, USA. · Curr Neurol Neurosci Rep. · Pubmed #12583848 No free full text.

Abstract: Disorders of sleep and daytime alertness are frequent in Parkinson's disease patients and arise from a number of diverse factors. The most common complaint of night-time sleep disturbance in Parkinson's disease is sleep fragmentation. Sleep fragmentation can be associated with recurrent parkinsonian symptoms, the effect of medications, concomitant medical disorders such as nocturia, or psychiatric disorders such as depression or anxiety. Likewise, nocturnal sleep disturbance may arise from sleep apnea, periodic limb movements of sleep, or rapid eye movement (REM) sleep behavior disorder. Nocturnal sleep deprivation may lead to excessive daytime sleepiness. Other potential sources of daytime sleepiness include the effects of medications or disruption of central sleep mechanisms due to the pathologic processes of Parkinson's disease itself. Diagnosis of sleep disturbances and daytime sleepiness requires a direct interview of the patient and the caregiver, and may involve consultation with the sleep specialist or medical physician. Treatment is aimed toward improving night-time sleep and daytime drowsiness by addressing the causative factors.

Factor SA, Feustel PJ, Friedman JH, Comella CL, Goetz CG, Kurlan R, Parsa M, Pfeiffer R, Anonymous00282. · Albany Medical Center, NY 12205, USA. · Neurology. · Pubmed #12796526 No free full text.

Abstract: OBJECTIVES: To examine the long-term outcome of PD patients with psychosis requiring antipsychotic therapy; to explore predictors of mortality, nursing home placement, dementia, and persistent psychosis; and to compare outcomes of those with persistent psychosis vs those whose psychosis resolved. METHODS: Baseline data available from 59 patients enrolled in the PSYCLOPS (PSychosis and CLOzapine in PD Study) trial included age, age at onset of PD, duration of PD and psychosis, character of psychosis, medications, living setting, and scores for Mini-Mental State Examination (MMSE), Unified Parkinson's Disease Rating Scale, Hoehn and Yahr Scale, and Clinical Global Impression Scale. Longitudinal data were collected 26 months later regarding four outcomes: death, nursing home placement, diagnosis of dementia, and persistence of psychosis. Logistic regression was used to explore whether any baseline characteristics were associated with an increased likelihood of one of these outcomes. RESULTS: At baseline, 56% of patients had an MMSE score of <25, 12% were in a nursing home, 95% had hallucinations, and 60% had paranoia. On follow-up, 25% were dead, nursing home placement occurred in 42%, psychosis was persistent in 69%, and dementia was diagnosed in 68%. Select baseline characteristics predicted individual outcomes: Nursing home placement was associated with the presence of paranoia and older age; persistent psychosis was associated with younger age at onset of PD and longer disease duration; dementia was associated with older age at PD onset and lower initial MMSE score; no characteristics predicted death. Whether psychosis persisted or not had no significant effect on the development of the other three outcomes. The prevalence of hallucinations at follow-up was not different between groups currently receiving antipsychotics vs those on no treatment. CONCLUSIONS: Psychosis in PD requiring antipsychotic therapy is frequently associated with death, nursing home placement, development and progression of dementia, and persistence of psychosis. Still, it appears the prognosis has improved with atypical antipsychotic therapy based on the finding that 28% of NH patients died within 2 years compared with 100% in a previous study done prior to availability of this treatment.

Nutt JG, Burchiel KJ, Comella CL, Jankovic J, Lang AE, Laws ER, Lozano AM, Penn RD, Simpson RK, Stacy M, Wooten GF, Anonymous00009. · Oregon Health & Science University, Portland 97201-3098, USA. · Neurology. · Pubmed #12525720 No free full text.

Abstract: OBJECTIVE: To assess the safety, tolerability, and biological activity of glial cell line-derived neurotrophic factor (GDNF) administered by an implanted intracerebroventricular (ICV) catheter and access port in advanced PD. BACKGROUND: GDNF is a peptide that promotes survival of dopamine neurons. It improved 6-OHDA- or MPTP-induced behavioral deficits in rodents and monkeys. METHODS: A multicenter, randomized, double-blind, placebo-controlled, sequential cohort study compared the effects of monthly ICV administration of placebo and 25, 75, 150, 300, and 500 to 4,000 microg of GDNF in 50 subjects with PD for 8 months. An open-label study extended exposure up to an additional 20 months and maximum single doses of up to 4,000 microg in 16 subjects. Laboratory testing, adverse events (AE), and Unified Parkinson's Disease Rating Scale (UPDRS) scoring were obtained at 1- to 4-week intervals throughout the studies. RESULTS: Twelve subjects received placebo and seven or eight subjects were assigned to each of the other GDNF dose groups. "On" and "off" total and motor UPDRS scores were not improved by GDNF at any dose. Nausea, anorexia, and vomiting were common hours to several days after injections of GDNF. Weight loss occurred in the majority of subjects receiving 75 microg or larger doses of GDNF. Paresthesias, often described as electric shocks (Lhermitte sign), were common in GDNF-treated subjects, were not dose related, and resolved on discontinuation of GDNF. Asymptomatic hyponatremia occurred in over half of subjects receiving 75 microg or larger doses of GDNF; it was symptomatic in several subjects. The open-label extension study had similar AE and lack of therapeutic efficacy. CONCLUSIONS: GDNF administered by ICV injection is biologically active as evidenced by the spectrum of AE encountered in this study. GDNF did not improve parkinsonism, possibly because GDNF did not reach the target tissues--putamen and substantia nigra.

Vaillancourt DE, Spraker MB, Prodoehl J, Abraham I, Corcos DM, Zhou XJ, Comella CL, Little DM. · Department of Kinesiology and Nutrition, University of Illinois at Chicago, 1919 West Taylor, 650 AHSB, MC 994, Chicago, IL 60612, USA. · Neurology. · Pubmed #19129507 No free full text.

Abstract: BACKGROUND: In the midbrain of patients with Parkinson disease (PD), there is a selective loss of dopaminergic neurons in the ventrolateral and caudal substantia nigra (SN). In a mouse model of PD, investigators have administered 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and found that measures derived using diffusion tensor imaging (DTI) were correlated with the number of dopamine neurons lost following intoxication. METHODS: Twenty-eight subjects (14 with early stage, untreated PD and 14 age- and gender-matched controls) were studied with a high-resolution DTI protocol at 3 Tesla using an eight-channel phase array coil and parallel imaging to study specific segments of degeneration in the SN. Regions of interest were drawn in the rostral, middle, and caudal SN by two blinded and independent raters. RESULTS: Fractional anisotropy (FA) was reduced in the SN of subjects with PD compared with controls (p < 0.001). Post hoc analysis identified that reduced FA for patients with PD was greater in the caudal compared with the rostral region of interest (p < 0.00001). A receiver operator characteristic analysis in the caudal SN revealed that sensitivity and specificity were 100% for distinguishing patients with PD from healthy subjects. Findings were consistent across both raters. CONCLUSIONS: These findings provide evidence that high resolution diffusion tensor imaging in the substantia nigra distinguishes early stage, de novo patients with Parkinson disease (PD) from healthy individuals on a patient by patient basis and has the potential to serve as a noninvasive early biomarker for PD.

Robichaud JA, Pfann KD, Leurgans S, Vaillancourt DE, Comella CL, Corcos DM. · Department of Kinesiology and Nutrition (M/C 994), University of Illinois at Chicago, 1919 West Taylor Street, 650 AHSB, MC 994, Chicago, IL 60612, USA. · Clin Neurophysiol. · Pubmed #19084473 No free full text.

Abstract: OBJECTIVE: This study evaluated whether changes in the electromygraphic (EMG) pattern during rapid point-to-point movements in individuals diagnosed with PD can: (1) distinguish PD subjects from healthy subjects and (2) determine if differences in the EMG pattern reflect disease severity in PD. METHODS: Three groups of 10 PD subjects and 10 age/sex-matched healthy subjects performed rapid 72 degree point-to-point elbow flexion movements. PD subjects were divided, a priori, into three groups based upon off medication motor UPDRS score. RESULTS: Measures related to the EMG pattern distinguished all PD subjects and 9 out of 10 healthy subjects, resulting in 100% sensitivity. Further, significant correlations were shown between EMG measures and the motor UPDRS score. After 30 months, the one healthy subject whose EMG pattern was abnormal was reexamined. The EMG measures remained abnormal and the motor UPDRS score went from 0 to 10. Parkinson's disease was diagnosed. CONCLUSION: Measures related to the variability of the EMG pattern during rapid point-to-point movements provide neurophysiological measures that objectively distinguish PD subjects from healthy subjects. These measures also correlate with disease severity. SIGNIFICANCE: EMG measures may provide a non-invasive measure that is sensitive and specific for identifying individuals with PD.

Schifitto G, Friedman JH, Oakes D, Shulman L, Comella CL, Marek K, Fahn S, Anonymous00354. · University of Rochester, NY, USA. · Neurology. · Pubmed #18695158 No free full text.

Abstract: BACKGROUND: Fatigue is a common complaint in Parkinson disease (PD). We investigated fatigue in a cohort of previously untreated patients with early PD enrolled in the Earlier vs Later Levodopa (ELLDOPA) clinical trial. METHODS: A total of 361 patients were enrolled in the randomized, double-blind, placebo-controlled ELLDOPA trial and assigned to receive placebo or carbidopa-levodopa 37.5/150 mg, 75/300 mg, or 150/600 mg daily for 40 weeks, followed by a 2-week medication washout period. Subjects who scored >4 on the Fatigue Severity Scale were classified as fatigued. PD severity was assessed using the Unified Parkinson's Disease Rating Scale (UPDRS), Hoehn-Yahr scale, and Schwab-England Activities of Daily Living Scale. A subgroup of subjects underwent [(123)I]-beta-CIT SPECT to measure striatal dopamine transporter density. RESULTS: Of the 349 ELLDOPA subjects who completed fatigue measures, 128 were classified as fatigued at baseline. The fatigued group was significantly more impaired neurologically (UPDRS, all subscales and Hoehn and Yahr staging) and functionally (Schwab-England Scale) but no significant differences were observed in beta-CIT measurements between the two groups. Analysis of covariance showed a greater increase in fatigue score from baseline to the end of the 2-week washout in the placebo group (0.75 points) than in the three groups receiving levodopa (increases of 0.30 [150 mg/day], 0.36 [300 mg/day], and 0.33 [600 mg/day]; p = 0.03 for heterogeneity). CONCLUSIONS: Fatigue is a frequent symptom in early, untreated, non-depressed patients with Parkinson disease (PD), affecting over 1/3 of the patients in this cohort at baseline and 50% by week 42. Fatigue was associated with the severity of PD, and progressed less in patients treated with levodopa.

Park M, Comella CL, Leurgans SE, Fan W, Wilson RS, Bennett DA. · Sleep Disorders Center, Rush University Medical Center, 710 South Paulina Street, JRB 6th Floor, Chicago, IL 60612, USA. · Sleep Med. · Pubmed #17023213 No free full text.

Abstract: BACKGROUND AND PURPOSE: Excessive daytime sleepiness (EDS) is reported in Alzheimer's disease (AD), with unstable sleep-wake rhythms that worsen with advancing disease stage. EDS is also very common in Parkinson's disease (PD), regardless of disease severity. The purpose of this study was to determine whether more Parkinsonian motor signs exist in AD patients with more reported daytime napping compared to AD patients without daytime napping. PATIENTS AND METHODS: AD patients ((National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer's Disease and Related Disorders Association) NINCDS/ADRDA criteria) were prospectively evaluated in a dementia clinic. Parkinsonian motor signs were assessed using a modified motor Unified Parkinson's Disease Rating Scale (mmUPDRS). AD patients were grouped according to daytime napping frequency: (1) minimal napping (AD-Naps), or (2) napping at least once a day (AD+Naps). Wilcoxon rank-sum tests and chi2-tests computed differences between groups for mmUPDRS, nighttime sleep disturbances, and the Mini Mental State Examination (MMSE). Statistical significance was set at P<0.05. RESULTS: AD patients were classified as AD-Naps (n=155) or AD+Naps (n=180). Compared with AD-Naps patients, AD+Naps patients had higher total mmUPDRS scores (P<0.001), higher rigidity scores (P<0.005), and more gait impairment (P<0.001). CONCLUSION: AD patients with more reported daytime napping had more Parkinsonian motor signs, suggesting that this subgroup may have an increased propensity for sleepiness resembling PD. Longitudinal studies with objective measures are needed to determine whether causal relationships exist between sleepiness and Parkinsonism in AD.

Comella CL, Morrissey M, Janko K. · Department of Neurologic Sciences, Rush University Medical Center, 1725 W. Harrison, Chicago, IL 60612, USA. · Neurology. · Pubmed #15851743 No free full text.

Abstract: Pergolide is a dopamine agonist that improves Parkinson disease but is associated with dose-dependent sleepiness. This study evaluates the effect of a nighttime dose of 1 mg of pergolide on actigraphic measures of sleep using a randomized, double-blind, placebo-controlled study design. The pergolide group (n = 10) worsened in actigraphic measures of sleep efficiency and sleep fragmentation vs the placebo group (n = 12). Side effects were more frequent in the pergolide group.

Robichaud JA, Pfann KD, Vaillancourt DE, Comella CL, Corcos DM. · Department of Physical Therapy, School of Health and Rehabilitation Sciences, Indiana University, Indianapolis, Indiana 46202, USA. · Mov Disord. · Pubmed #15593316 No free full text.

Abstract: Several measures of isometric contractions reflect motor impairments in subjects with Parkinson's disease (PD), including long relaxation times and greater power in the 5 to 15 Hz electromyographic (EMG) bandwidth during the holding phase of contractions compared to those measures in healthy subjects. We sought to determine whether the impairments observed in subjects with PD in the performance of isometric contractions reflect disease severity. Twenty-eight subjects with PD performed isometric contractions at a torque level equal to 50% of the torque generated during a maximum voluntary contraction while off medication. Subjects were instructed to reach the target torque as fast as possible upon hearing the auditory "go" signal and to relax their muscles when a second auditory cue signaled the end of the hold phase. There was a significant positive correlation between torque relaxation time and Unified Parkinson's Disease Rating Scale (UPDRS)-Motor score. A significant positive correlation was also observed between the proportion of power in the 5 to 15 Hz frequency bin of the agonist EMG signal and UPDRS-Motor score, and a significant negative correlation between the proportion of power in the 15 to 30 Hz frequency bin and UPDRS-Motor score. These measures provide objective quantification of the severity of motor impairment that can be used to investigate the efficacy of different interventions in individuals with PD.

Pfann KD, Robichaud JA, Gottlieb GL, Comella CL, Brandabur M, Corcos DM. · The Department of Movement Science (M/C 194), University of Illinois at Chicago, 901 West Roosevelt Road, Chicago, IL 60608, USA. · Exp Brain Res. · Pubmed #14991213 No free full text.

Abstract: When young, healthy subjects perform rapid point-to-point and reversal movements over a range of distances, the patterns of muscle activation associated with accelerating the limb toward the target are modulated in the same way for both movement tasks. Differences in patterns of muscle activation for these two movement types are not observed until the deceleration phase of the movements. In this study, we first test the hypothesis that healthy, older subjects and subjects with Parkinson's disease will modulate the pattern of muscle activation in the same way during the acceleration phase of point-to-point and reversal elbow movements. Second, we test the hypothesis that healthy, older subjects and subjects with Parkinson's disease exhibit the same relationship in muscle activation patterns between the two movement types that have been observed for the young in the deceleration phase of the movements. Subjects performed point-to-point and reversal movements initiated in the direction of flexion over three distances (36, 54 and 72 degrees) "as fast as possible". Angle, velocity, acceleration and surface EMGs from biceps and triceps were recorded. With respect to the first hypothesis, the EMG, kinetic, and kinematic measures related to the acceleration phase of the movements were modulated in the same way for both movement types in the healthy older subjects. In the Parkinson's disease group, the kinematic and kinetic measures during the acceleration phase of the movements were the same in both movement types; however, the flexor and extensor EMG activation was smaller during reversal movements than during point-to-point movements. With respect to the second hypothesis, in contrast to that found in young subjects, in healthy older subjects, there was no significant difference between the movement types in the flexor EMG activity immediately after the time of peak velocity. This difference between younger and older subjects may be attributed to the fact that older subjects perform both movement types more slowly than do younger subjects. Although subjects with Parkinson's disease also move slowly, the flexor EMG shuts off more abruptly and more completely just after the time of peak velocity during reversal movements than during point-to-point movements. These results show that (1) for healthy subjects, when the task requirements are the same for the two movement types (acceleration phase), muscle activation patterns are modulated in the same way, and (2) both age and disease alter the relationship of muscle activation, kinetics and kinematics between point-to-point and reversal movements.

Robichaud JA, Pfann KD, Comella CL, Brandabur M, Corcos DM. · Department of Human Movement Sciences (M/C 194), University of Illinois at Chicago, 901 West Roosevelt Road, Chicago, IL 60608, USA. · Exp Brain Res. · Pubmed #14747885 No free full text.

Abstract: Research on isometric contractions in subjects with Parkinson's disease (PD) has shown that anti-parkinsonian medication results in a greater increase in extensor strength than flexor strength. This finding is consistent with the hypothesis that there is a greater impairment in neural activation of extensor muscles as compared to flexor muscles in subjects with PD. Such a hypothesis is physiologically feasible given the known differences in the neural control of flexor and extensor muscles. If the above hypothesis is true for both phasic and tonic muscle activation, then differences between performance of rapid single-joint flexion and extension movements should exist in subjects with PD. Twelve subjects with PD, "off" and "on" medication, and 12 age-and sex-matched healthy control subjects performed rapid single-joint movements in flexion and extension over three distances. For neurologically healthy subjects, we did not identify any significant differences in either kinematic or EMG parameters between flexion and extension movements. In contrast, in the PD subjects extension movements were slower and associated with more agonist bursts when compared to flexion movements. The results are consistent with the hypothesis that there is a differential impairment of neural activation of extensor muscles of the arm as compared to flexor muscles in subjects with PD.

Robichaud JA, Pfann KD, Comella CL, Corcos DM. · School of Kinesiology, University of Illinois at Chicago, Chicago, Illinois 60608, USA. · Mov Disord. · Pubmed #12360544 No free full text.

Abstract: Individuals with Parkinson's disease show dramatic improvements in their ability to move when medicated. However, the neural cause of this improvement is unclear. One hypothesis is that neural activation patterns, as measured by surface electromyography (EMG), are normalized by medication. We tested this hypothesis by investigating the effect of medication on the electromyographic (EMG) patterns recorded when individuals with idiopathic Parkinson's disease performed elbow flexion movements over three movement distances while off and on antiparkinsonian medication. When the subjects were off medication, they lacked the ability to modulate the agonist EMG burst duration with changes in movement distance. The ability to modulate agonist EMG burst duration is characteristic of the EMG patterns observed in healthy subjects. Also, multiple agonist bursts were exhibited during the acceleration phase. As expected, medication diminished the clinical signs of Parkinson's disease, increased movement speed, and increased the magnitude of the first agonist burst. Medication did not restore agonist burst duration modulation with movement distance, did not change the frequency of agonist bursting, and did not alter the timing of the antagonist activation. These results show that medication does not alter the temporal profile of EMG activation.

Pfann KD, Buchman AS, Comella CL, Corcos DM. · School of Kinesiology, University of Illinois at Chicago, 60608-1516, USA. · Mov Disord. · Pubmed #11748736 No free full text.

Abstract: Studies of electromyographic (EMG) patterns during movements in Parkinson's disease (PD) have often yielded contradictory results, making it impossible to derive a set of rules to explain how muscles are activated to perform different movement tasks. We sought to clarify the changes in modulation of EMG parameters associated with control of movement distance during fast movements in patients with PD. Specifically, we studied surface EMG activity during rapid elbow flexion movements over a wide range of distances (5-72 degrees) in 14 patients with relatively mild symptoms of PD and 14 control subjects of similar age, sex, height, and weight. The PD group exhibited several changes in EMG modulation including impaired modulation of agonist burst duration; increased number of agonist bursts; reduced scaling of agonist EMG magnitude in the more severely impaired subjects; and increased temporal overlap of the antagonist and agonist signals in the most severely impaired subjects. These findings suggest that progressive motor dysfunction in PD is accompanied by increasing deficits in modulating muscle activation. These results help clarify previous disparate and sometimes contradictory results of EMG patterns in subjects with PD.

Kompoliti K, Comella CL, Jaglin JA, Leurgans S, Raman R, Goetz CG. · Department of Neurological Sciences, Rush-Presbyterian-St Luke's Medical Center, Rush University, Chicago, IL, USA. · Neurology. · Pubmed #11094119 No free full text.

Abstract: Questionnaire studies have found that parkinsonism worsens in women during the premenstrual period, when estrogen and progesterone levels are presumably at their nadir. To assess this patient-based observation and correlate motor signs with hormonal levels, the authors prospectively studied 10 menstruating women with PD in their "off" state, on 5 successive weeks. Although PD severity fluctuated during the study period, there was no significant correlation between the objective or subjective measures of parkinsonism and estrogen and progesterone levels.