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Cynthia L Comella

Publications and source records attributed to Cynthia L Comella.

18 recordsLinked to original sources
PubMed2006

Association of daytime napping and Parkinsonian signs in Alzheimer's disease.

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.

Adult↗
PubMed2006

Rate of force production and relaxation is impaired in patients with focal hand dystonia.

One factor, which may contribute to slowed movement in dystonia, is impairment in controlling the voluntary rate of motor output. This study examined the ability of patients with focal hand dystonia to rapidly turn force on and off at the wrist and elbow joints. Dystonic patients were slower than controls in rapidly turning on force from rest at both joints, passively relaxing force and rapidly reversing force output from a steady-state flexion contraction. Adding a preload did not improve the ability of dystonic subjects to rapidly turn on force. These results support the idea that dystonia is a disorder of impaired motor cortical activation, possibly due to basal ganglia dysfunction.

Adult↗
PubMed2006

Strength deficits in primary focal hand dystonia.

Cortical activation is reduced when patients with focal dystonia perform movements that do not induce dystonic posturing. This finding suggests that the cortical drive to muscles may in some circumstances actually be reduced not increased, as suggested by basal ganglia models of dystonia as a hyperkinetic disorder. The purpose of this study was to examine flexor and extensor strength at the wrist (a clinically affected joint) and elbow (a nonclinically affected joint) in 18 patients with primary focal hand dystonia compared to matched control subjects. We measured peak torque from maximum voluntary contractions, and agonist and antagonist muscle activation by means of surface electromyograms. Patients were significantly weaker than controls at both the elbow and wrist joints and in both flexors and extensors compared to controls. Peak elbow flexion torque was, on average, 14.4% lower in the dystonic compared to the control group, elbow extensor peak torque was 28.6% lower, wrist flexor peak torque was 17.4% lower, and wrist extensor peak torque was 20.7% lower. Strength did not differ as a function of clinical severity. Reductions in peak torque were accompanied by reduced agonist activation, although this finding only reached statistical significance at the elbow. The amount of co-contraction of antagonistic muscles was not significantly different between the two groups. These results are discussed in the context of dystonia as a disorder resulting from dysfunction of basal ganglia output.

Adult↗
PubMed2005

Nocturnal activity with nighttime pergolide in Parkinson disease: a controlled study using actigraphy.

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.

Age Factors↗
PubMed2005

Force control and disease severity in Parkinson's disease.

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.

Acoustic Stimulation↗
PubMed2005

Efficacy and safety of botulinum type A toxin (Dysport) in cervical dystonia: results of the first US randomized, double-blind, placebo-controlled study.

Botulinum toxin type A (Dysport) has been shown in European studies to be a safe and effective treatment for cervical dystonia. This multicenter, double-blind, randomized, controlled trial assessed the safety and efficacy of Dysport in cervical dystonia patients in the United States. Eighty patients were randomly assigned to receive one treatment with Dysport (500 units) or placebo. Participants were followed up for 4 to 20 weeks, until they needed further treatment. They were assessed at baseline and weeks 2, 4, 8, 12, 16, and 20 after treatment. Dysport was significantly more efficacious than placebo at weeks 4, 8, and 12 as assessed by the Toronto Western Spasmodic Torticollis Rating Scale (10-point vs. 3.8-point reduction in total score, respectively, at week 4; P < or = 0.013). Of participants in the Dysport group, 38% showed positive treatment response, compared to 16% in the placebo group (95% confidence interval, 0.02-0.41). The median duration of response to Dysport was 18.5 weeks. Side effects were generally similar in the two treatment groups; only blurred vision and weakness occurred significantly more often with Dysport. No participants in the Dysport group converted from negative to positive antibodies after treatment. These results confirm previous reports that Dysport (500 units) is safe, effective, and well-tolerated in patients with cervical dystonia.

Adult↗
PubMed2005

Rating scale for psychogenic movement disorders: scale development and clinimetric testing.

We developed and tested the clinimetric properties of a scale for psychogenic movement disorders (PMDs). PMDs are disabling but lack any generally accepted treatment strategies. To develop treatments, means of assessing disease severity must be provided. No scale to assess PMDs existed. The PMD scale developed here rates 10 phenomena (rest tremor, action tremor, dystonia, chorea, bradykinesia, myoclonus, tics, athetosis, ballism, cerebellar incoordination), 2 functions (gait, speech), and 14 body regions. To study interrater agreement, three movement disorder neurologists independently rated 88 videotapes of PMD patients. Data analysis was performed using a kappa coefficient of agreement, Kendall's coefficient of concordance, Spearman correlations, and intraclass correlation coefficients. Validity and scale responsiveness were tested as well. All phenomena and speech and gait dysfunction occurred in the patient sample. A wide range of affected body regions, severity, and incapacitation was captured. Ratings showed excellent interrater reliability for presence or absence of each phenomenon (kappa range, 0.63 to 0.86). Kendall's concordance coefficients for phenomenology, function, and total PMD scores were 0.92, 0.93, and 0.91. Spearman correlations between raters ranged from 0.86 to 0.90. The scale was responsive to changes that occurred as a result of a neuropsychiatric intervention. The PMD scale adequately captures the complex movements of PMDs and can be used to assess PMDs and test the efficacy of intervention strategies.

Adolescent↗
PubMed2005

Restless legs syndrome.

RLS is a common condition that is likely to be encountered by primary care physicians in their practice. The currently available medications are highly effective in treating RLS. The knowledge of clinical presentation and diagnostic features of RLS will empower the primary care practitioners to effectively treat their patients who have RLS.

Dopamine Agonists↗
PubMed2004

Greater impairment of extension movements as compared to flexion movements in Parkinson's disease.

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.

Aged↗
PubMed2004

Botulinum toxins in neurological disease.

Botulinum toxins are among the most potent neurotoxins known to humans. In the past 25 years, botulinum toxin has emerged as both a potential weapon of bioterrorism and as a powerful therapeutic agent, with growing applications in neurological and non-neurological disease. Botulinum toxin is unique in its ability to target peripheral cholinergic neurons, preventing the release of acetylcholine through the enzymatic cleavage of proteins involved in membrane fusion, without prominent central nervous system effects. There are seven serotypes of the toxin, each with a specific activity at the molecular level. Currently, serotypes A (in two preparations) and B are available for clinical use, and have been shown to be safe and effective for the treatment of dystonia, spasticity, and other disorders in which muscle overactivity gives rise to symptoms. This review focuses on the pharmacology, electrophysiology, immunology, and application of botulinum toxin in selected neurological disorders.

Animals↗
PubMed2003

Rating scales for dystonia: a multicenter assessment.

The evaluation of dystonia requires a reliable rating scale. The widely used Fahn-Marsden Scale (F-M) has not been sufficiently tested across multiple centers and investigators. The Dystonia Study Group developed the Unified Dystonia Rating Scale (UDRS) and a Global Dystonia Rating Scale (GDS) to serve as instruments to assess dystonia severity. In this study, 25 dystonia experts evaluated the UDRS, F-M, and GDS for internal consistency and reliability. One hundred dystonia patients were videotaped using a standardized videotape protocol. Each examiner rated 20 patients using the UDRS, F-M, and GDS in random order. The examiner then assessed each scale for ease of use. Statistical analysis used Cronbach's alpha, intraclass correlation coefficients (ICC), generalized weighted kappa statistic, and Kendall's coefficient of concordance. The UDRS, F-M, and GDS showed excellent internal consistency (Cronbach's alpha 0.89-0.93) and good to excellent correlation among the raters (ICC range from 0.71-0.78). Inter-rater agreement was fair to excellent (Kendall's 0.54-0.87; kappa 0.37-0.91) being lowest for eyes, jaw, face, and larynx. The modifying ratings (Duration in the UDRS and Provoking Factor in the F-M) showed less agreement than the motor severity ratings. Among scales, the total scores correlated (Pearson's r, 0.977-0.983). Overall, 74% of raters found the GDS the easiest to apply. The GDS with its simplicity and ease of application may be the most useful dystonia rating scale.

Dystonia↗
PubMed2003

Sleep disturbances in Parkinson's disease.

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.

Antiparkinson Agents↗
PubMed2003

Benefits and risks of pharmacological treatments for essential tremor.

Essential tremor can cause significant functional disability in some patients. The arms are the most common body part affected and cause the most functional disability. The treatment of essential tremor includes medications, surgical options and other forms of therapy. Presently there is no cure for essential tremor nor are there any medications that can slow the progression of tremor. Treatment for essential tremor is recommended if the tremor causes functional disability. If the tremor is disabling only during periods of stress and anxiety, propranolol and benzodiazepines can be used during those periods when the tremor causes functional disability. The currently available medications can improve tremor in approximately 50% of the patients. If the tremor is disabling, treatment should be initiated with either primidone or propranolol. If either primidone or propranolol do not provide adequate control of the tremor, then the medications can be used in combination. If patients experience adverse effects with propranolol, occasionally other beta-adrenoceptor antagonists (such as atenolol or metoprolol) can be used. If primidone and propranolol do not provide adequate control of tremor, occasionally the use of benzodiazepines (such as clonazepam) can provide benefit. Other medications that may be helpful include gabapentin or topiramate. If a patient has disabling head or voice tremor, botulinum toxin injections into the muscles may provide relief from the tremor. Botulinum toxin in the hand muscles for hand tremor can result in bothersome hand weakness and is not widely used. There are other medications that have been tried in essential tremor and have questionable efficacy. These drugs include carbonic anhydrase inhibitors (e.g. methazolamide), phenobarbital, calcium channel antagonists (e.g. nimodipine), isoniazid, clonidine, clozapine and mirtazapine. If the patient still has disabling tremor after medication trials, surgical options are usually considered. Surgical options include thalamotomy and deep brain stimulation of the thalamus. These surgical options provide adequate tremor control in approximately 90% of the patients. Surgical morbidity and mortality for these procedures is low. Deep brain stimulation and thalamotomy have been shown to have comparable efficacy but fewer complications have been reported with deep brain stimulation. In patients undergoing bilateral procedures deep brain stimulation of the thalamus is the procedure of choice to avoid adverse effects seen with bilateral ablative procedures. The use of medication and/or surgery can provide adequate tremor control in the majority of the patients.

Adrenergic Agonists↗
PubMed2002

Restless legs syndrome: treatment with dopaminergic agents.

Restless legs syndrome (RLS) is a common neurologic disorder that affects 5 to 10% of the population and increases in prevalence with aging. The clinical hallmarks of RLS include dysesthesias or paresthesias in the legs and sometimes the arms, occurring primarily at rest, which are usually worse in the evening and are alleviated by movement. RLS can be a disabling disorder, causing sleep disturbance at night and excessive sleepiness during the day. Although treatment with levodopa alleviates symptoms, many RLS patients develop rebound (occurrence of symptoms during the night) or augmentation (occurrence of symptoms before levodopa dosing in the evening). Augmentation occurs in up to 82% of patients treated with levodopa, limiting the long-term usefulness of this agent. The direct dopamine receptor agonists are long-acting drugs often administered as a single dose at bedtime. Among these agents, pergolide, pramipexole, ropinirole, and cabergoline have all been shown to alleviate RLS symptoms in 70 to 100% of patients. The most common adverse effect is nausea. Augmentation, although it may be associated with chronic agonist use, is usually mild and responsive to additional dosing. The direct dopamine receptor agonists have largely replaced levodopa as the most effective treatment for RLS.

Clinical Trials as Topic↗
PubMed2002

Effect of medication on EMG patterns in individuals with Parkinson's disease.

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.

Aged↗
PubMedDate not supplied

Treatment of dystonia.

Therapeutic strategies in the treatment of dystonia consist primarily of pharmacologic, surgical, and supportive approaches. Many recent advances have been made in the treatment of dystonia with newer medications, availability of different botulinum toxins, and surgical procedures. However, these treatment modalities all have limiting factors and varying levels of efficacy. Studies range from case reports and open-label trials to double-blind placebo-controlled trials. More research and larger studies are needed to explore these newer medications and surgical techniques for both primary focal and generalized dystonia. Studies in functional outcome and quality of life further support the importance of discovering safe and effective means to treat dystonia. An algorithmic approach may be useful to guide the physician along the various treatment choices.

Animals↗