<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_425"
                     title="AAN: Industrial Cleaner Again Tied to Parkinson Risk (CME/CE)"
                     score="0.015"
                     href="http://www.medpagetoday.com/MeetingCoverage/AAN/tb/18338?impressionId=1265746168761"
                     
      TORONTO  --  The degreasing agent trichloroethylene (TCE) has been linked to increased rates of Parkinson&apos;s disease among industrial workers in yet another study, this time involving a large, well-studied group of World War II veterans.&lt;br&gt;
&lt;br&gt;Parkinson&apos;s disease developed in individuals with occupational exposure to TCE at more than five times the rate seen in those without such exposure (odds ratio 5.5, 95% CI 1.02 to 30), reported Samuel Goldman, MD, of the Parkinson&apos;s Institute in Sunnyvale, Calif.&lt;br&gt;
&lt;br&gt;Goldman described the research in a phone interview with &lt;em&gt;MedPage Today&lt;/em&gt;. It&apos;s scheduled for presentation here in April at the American Academy of Neurology&apos;s annual meeting.&lt;br&gt;
&lt;br&gt;A previous study in 2008 had fingered TCE as the most likely culprit behind a cluster of Parkinson&apos;s disease cases afflicting workers at a single industrial plant. (See &lt;a href=&quot;http://www.medpagetoday.com/Geriatrics/ParkinsonsDisease/7894&quot; mce_href=&quot;http://www.medpagetoday.com/Geriatrics/ParkinsonsDisease/7894&quot; target=&quot;_blank&quot;&gt;Trichloroethylene Implicated as Risk for Parkinsonism&lt;/a&gt;)&lt;p&gt;&lt;/p&gt;
&lt;p&gt;Also, Goldman said, animal studies have found that TCE is selectively toxic to nigral dopaminergic neurons, the same type of nerve cell that progressively dies off in Parkinson&apos;s disease. He said the chemical&apos;s activity in rodent brains is very similar to that of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a dopaminergic neurotoxin commonly used to simulate Parkinson&apos;s disease in preclinical research.&lt;/p&gt;
&lt;p&gt;Goldman said the new study was the first population-based analysis to link TCE to the disease.&lt;/p&gt;
&lt;p&gt;It focused on 198 twin pairs in the National Academy of Sciences-National Research Council&apos;s World War II Twins Cohort, which comprises some 16,000 twin pairs overall.&lt;/p&gt;
&lt;p&gt;Members of the all-male cohort, who were born from 1917 to 1927 and served in the war, have been followed since the 1960s. Occupational histories for participants are available along with medical records from the VA healthcare system.&lt;/p&gt;
&lt;p&gt;In those pairs chosen for the current study, records showed that one twin had developed Parkinson&apos;s disease and the other had not. This design largely eliminates genetics as a confounding factor in the analysis.&lt;/p&gt;
&lt;p&gt;Goldman explained that occupational histories for each participant were reviewed by a blinded industrial hygienist and a preventive medicine physician to identify likely exposures to TCE and four other industrial chemicals: xylene, toluene, carbon tetrachloride, and tetrachloroethylene.&lt;/p&gt;
&lt;p&gt;As a single source of exposure, only TCE was significantly associated with development of Parkinson&apos;s disease, Goldman said.&lt;/p&gt;
&lt;p&gt;People working as aircraft mechanics, machinists, plumbers, and electricians likely had regular exposure to TCE, Goldman said. The chemical was commonly used as a &quot;spot&quot; cleaner to remove grease and oils from metal surfaces. It was also used for a time as a dry cleaning solvent, although tetrachloroethylene was more common for that purpose.&lt;/p&gt;
&lt;p&gt;Goldman said no increased risk was seen with xylene or toluene, but there were near-significant trends toward increased Parkinson&apos;s disease risk from carbon tetrachloride and tetrachloroethylene: &lt;ul&gt; &lt;li&gt;Carbon tetrachloride: OR 2.8 (95% CI 0.97 to 7.8)&lt;/li&gt; &lt;li&gt;Tetrachloroethylene: OR 9.0 (95% CI 0.78 to 103)&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;Twins exposed to either TCE or tetrachloroethylene were at significantly increased risk, with an odds ratio of 8.1 (95% CI 1.43 to 43) relative to individuals with no exposure to either chemical.&lt;/p&gt;
&lt;p&gt;Goldman said the analysis also examined whether duration of exposure was associated with increased risk. He said the results were in the same pattern as for the yes-no exposure analysis, but the findings were very uncertain because of the relatively small sample size.&lt;/p&gt;
&lt;p&gt;Occupational histories were available for only 99 of the 198 discordant twin pairs and some of the information was obtained by proxy rather than from the participant himself.&lt;/p&gt;
&lt;p&gt;Because of the wide confidence intervals even for the yes-no exposure analysis, the findings need confirmation in a larger study, he said, noting that the best approach would be a cohort study involving people with known, long-term exposure to TCE, compared with well-chosen controls.&lt;/p&gt;
&lt;p&gt;&quot;The study wouldn&apos;t have to be large,&quot; Goldman said. He estimated that 1,000 to 2,000 participants would be adequate to determine if the connection to Parkinson&apos;s disease is real.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was funded by the National Institute of Neurological Disorders and Stroke, the Valley Foundation, and the James and Sharron Clark Family Fund.&lt;/p&gt;&lt;p&gt;No potential conflicts of interest were reported.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_206"
                     title="Treadmill Training Improves Walking in Parkinson&apos;s (CME/CE)"
                     score="-0"
                     href="http://www.medpagetoday.com/Neurology/ParkinsonsDisease/tb/18049?impressionId=1265746168761"
                     
      Treadmill training can improve the impaired walking associated with Parkinson&apos;s disease, researchers said.&lt;br&gt;
&lt;br&gt;The technique leads to improvements in gait speed, stride length, and walking distance, but not gait cadence, according to Jan Mehrholz, PhD, of the Klinik Bavaria in Kreischa, Germany, and colleagues.&lt;br&gt;
&lt;br&gt;However, it remains unclear how long such improvements last, the researchers noted in a &lt;em&gt;Cochrane Systematic Review&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;Treadmill training has emerged recently as a &quot;promising investigational therapy&quot; aimed at patients with weakness on one side of the body and impaired gait, Mehrholz and colleagues wrote in their review.&lt;br&gt;
&lt;br&gt;To evaluate what&apos;s known about the subject, the researchers searched the literature and found eight randomized, controlled studies with a total of 203 participants.&lt;/p&gt;
&lt;p&gt;On average, patients were 61, with an average duration of disease in the studies ranging from one to eight years.&lt;/p&gt;
&lt;p&gt;When the studies were analyzed, the researchers found: 


&lt;table style=&quot;color: #151515; line-height: 16px; font: normal 14px Arial;&quot;&gt;
                &lt;tr&gt;&lt;td valign=&quot;top&quot;&gt;&lt;li&gt;&lt;/li&gt;&lt;/td&gt; &lt;td&gt;Seven studies  --  with153 participants all told  --  found that treadmill training improved gait speed. The pooled standardized mean difference was 0.50, which was significant at &lt;em&gt;P&lt;/em&gt;=0.003.&lt;/td&gt;&lt;/tr&gt;
                &lt;tr&gt;&lt;td valign=&quot;top&quot;&gt;&lt;li&gt;&lt;/li&gt;&lt;/td&gt; &lt;td&gt;Five studies, with a total of 95 participants, looked at stride length and found that treadmill training was beneficial. The pooled standardized mean difference was 0.50, which was significant at &lt;em&gt;P&lt;/em&gt;=0.05.&lt;/td&gt;&lt;/tr&gt;
                &lt;tr&gt;&lt;td valign=&quot;top&quot;&gt;&lt;li&gt;&lt;/li&gt;&lt;/td&gt; &lt;td&gt;Two studies, with 41 participants, found that treadmill training improved walking distance. The mean difference was 358 meters, which was significant at &lt;em&gt;P&lt;/em&gt;&amp;lt;0.0001.&lt;/td&gt;&lt;/tr&gt;
&lt;tr&gt;&lt;td valign=&quot;top&quot;&gt;&lt;li&gt;&lt;/li&gt;&lt;/td&gt; &lt;td&gt;Finally, four studies (with 78 participants) found no significant mean difference in cadence.&lt;/td&gt;&lt;/tr&gt;
              &lt;/table&gt;

&lt;p&gt;The treadmill training was acceptable to patients, the researchers said, in that it did not increase the risk of patients dropping out of studies. Adverse events were not reported.&lt;/p&gt;
&lt;p&gt;The researchers noted that the study protocols varied markedly.&lt;/p&gt;
&lt;p&gt;The treadmill training lasted from one 30-minute session to eight weeks, although most studies used a four-, six- or eight-week period. Frequency varied from a single session to four times a week, the researchers said.&lt;/p&gt;
&lt;p&gt;The type of treadmill training also varied, with some investigators using body-weight supported treadmill training and others a speed-dependent approach.&lt;/p&gt;
&lt;p&gt;Primary outcomes also differed, Mehrholz and colleagues said.&lt;/p&gt;
&lt;p&gt;Because of those variations, they said, there is &quot;still a need for well-designed large-scale studies&quot; to look at the risk and benefits of treadmill training for Parkinson&apos;s patients.&lt;/p&gt;
&lt;p&gt;Specifically, they said, those studies should address open questions about how long the effect lasts and what should be the frequency and duration of training.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was supported by the Klinik Bavaria Kreischa, the Technical University Dresden, SRH Fachhochschule Gera, and the California State University Long Beach.&lt;/p&gt;&lt;p&gt;Mehrholz and another author were co-authors of one included trial but did not participate in its quality assessment and data extraction.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_85"
                     title="PET Imaging Ups Diagnostic Accuracy in Parkinson&apos;s (CME/CE)"
                     score="-0.005"
                     href="http://www.medpagetoday.com/Neurology/ParkinsonsDisease/tb/17875?impressionId=1265746168761"
                     
      Metabolic brain imaging improved diagnostic accuracy by about 20% in patients with features of early parkinsonism but an uncertain clinical diagnosis, international researchers reported.&lt;br&gt;
&lt;br&gt;Writing online in &lt;em&gt;Lancet Neurology&lt;/em&gt;, Chris Tang, MD, of the Feinstein Institute for Medical Research in Manhasset, N.Y., and colleagues reported that image-based classification for idiopathic Parkinson&apos;s disease had 84% sensitivity, 97% specificity, 98% positive predictive value, and 82% negative predictive value.&lt;br&gt;
&lt;br&gt;In comparison to these high values, published clinicopathologic data suggest that the positive predictive value of a clinical diagnosis, even by a specialist, is only about 75%.&lt;/p&gt;
&lt;p&gt;Many neurodegenerative diseases share common signs and symptoms, and some 80% of patients misdiagnosed as having Parkinson&apos;s disease actually have multiple system atrophy or progressive supranuclear palsy.&lt;/p&gt;
&lt;p&gt;These conditions have a much worse prognosis than idiopathic Parkinson&apos;s disease, which does not substantially shorten lifespan.&lt;/p&gt;
&lt;p&gt;Moreover, treatments differ for these conditions, so more accurate diagnostic techniques have been needed.&lt;/p&gt;
&lt;p&gt;So Tang and colleagues employed an imaging technique known as fluorine-18-labeled-fluorodeoxyglucose (FDG)-PET to identify specific disease-related metabolic patterns for the three conditions.&lt;/p&gt;
&lt;p&gt;They noted that Parkinson&apos;s disease was characterized by increased pallidothalamic and pontocerebellar metabolic activity. Multiple system atrophy had bilateral reductions in putamen and cerebellar activity, and supranuclear palsy showed metabolic deficits in the upper brain stem, medial frontal cortex, and medial thalamus.&lt;/p&gt;
&lt;p&gt;Among 167 patients with parkinsonian features but uncertain clinical diagnosis who underwent FDG-PET, 96 were classified as having Parkinson&apos;s disease, 41 with multiple system atrophy, and 30 with progressive supranuclear palsy.&lt;/p&gt;
&lt;p&gt;Patients also were assessed clinically by blinded movement disorders specialists and followed for a mean of 2.6 years before a final clinical diagnosis was made.&lt;/p&gt;
&lt;p&gt;The investigators employed a multiple-pattern analytical technique to compute a patient&apos;s likelihood of having each disease, and calculated the discriminative measures for each.&lt;/p&gt;
&lt;p&gt;They found that the imaging classifications were accurate not only for idiopathic Parkinson&apos;s disease, but also for multiple system atrophy: &lt;ul&gt; &lt;li&gt;Sensitivity, 85%&lt;/li&gt; &lt;li&gt;Specificity, 96%&lt;/li&gt; &lt;li&gt;Positive predictive value, 97%&lt;/li&gt; &lt;li&gt;Negative predictive value, 83%&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;And for progressive supranuclear palsy: &lt;ul&gt; &lt;li&gt;Sensitivity, 88%&lt;/li&gt; &lt;li&gt;Specificity, 94%&lt;/li&gt; &lt;li&gt;Positive predictive value, 91%&lt;/li&gt; &lt;li&gt;Negative predictive value, 92%&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;They also calculated these discriminative values for patients with short duration of disease (less than two years), when it can be particularly difficult to make a diagnosis clinically because disease-specific features have not yet appeared.&lt;/p&gt;
&lt;p&gt;Patients with short duration of disease also would be &quot;ideal participants in clinical trials of potential disease-modifying drugs,&quot; the investigators noted.&lt;/p&gt;
&lt;p&gt;Among 55 patients with short-duration disease, the positive predictive values for idiopathic Parkinson&apos;s disease and atypical parkinsonian syndrome were 92% and 95%, respectively.&lt;/p&gt;
&lt;p&gt;And among 33 of these patients who were then followed for at least two years after imaging, the positive predictive values rose to 94% and 100%.&lt;/p&gt;
&lt;p&gt;This ability to make an imaging classification accurately several years before the final clinical diagnosis &quot;is especially relevant when considering treatment options for patients with medically refractory parkinsonism because invasive surgical approaches such as deep brain stimulation are generally ineffective for patients with atypical parkinsonian syndrome,&quot; the investigators wrote.&lt;/p&gt;
&lt;p&gt;Moreover, for patients with atypical parkinsonism, the high sensitivity and specificity &quot;will be of particular advantage when assessing potential participants in clinical trials of drugs to treat these progressive disorders.&quot;&lt;/p&gt;
&lt;p&gt;An accompanying editorial noted that the different types of parkinsonism cannot be classified with available techniques such as imaging of dopamine transporters with single-photon emission CT or of fluorodopa uptake with PET.&lt;/p&gt;
&lt;p&gt;&quot;The clinical and research relevance of these findings should not be underestimated,&quot; wrote Angelo Antonini, of IRCCS San Camillo, Venice and Parkinson Institute in Milan, Italy.&lt;/p&gt;
&lt;p&gt;&quot;Neuroprotective and disease-modifying drug research is intensifying and results mostly rely on accurate early diagnosis. If neuronal loss in Parkinson&apos;s disease follows a linear or exponential pattern, early treatment is crucial,&quot; Antonini argued.&lt;/p&gt;
&lt;p&gt;But advanced imaging should not be considered a replacement for thorough clinical investigation by movement disorder neurologists, and prospective multicenter studies are needed to confirm the accuracy of this metabolic pattern-based approach, he cautioned.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was funded by the National Institutes of Health and General Clinical Research Center at the Feinstein Institute for Medical Research.&lt;/p&gt;&lt;p&gt;One investigator holds patents for the use of spatial patterns in the diagnosis of brain disease, but has no financial conflicts of interest.&lt;/p&gt;&lt;p&gt;The editorialist declared no conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20090101_19_1839"
                     title="ICPDMD: Early Entacapone Doesn&apos;t Delay Dyskinesias in Parkinson&apos;s"
                     score="-0.005"
                     href="http://www.medpagetoday.com/Neurology/ParkinsonsDisease/tb/14626?impressionId=1265746168761"
                     
      PARIS, June 9 -- Adding entacapone (Comtan) to levodopa early in Parkinson&apos;s disease does not delay onset of dyskinesias, researchers said here.
              &lt;p&gt; 
              &lt;p&gt;Instead, and contrary to expectations, early entacapone hastened onset of dyskinesias, lead author C. Warren Olanow, M.D., of Mount Sinai School of Medicine in New York, told attendees at the International Congress of Parkinson&apos;s Disease and Movement Disorders.
              &lt;p&gt; 
              &lt;p&gt;Dyskinesias develop in most Parkinson&apos;s patients after five to 10 years of successful therapy with levodopa. Evidence indicates they may be caused by pulsatile dopaminergic stimulation, Dr. Olanow said, rather than the normal continuous stimulation produced by the healthy brain.
              &lt;p&gt; 
              &lt;p&gt;There&apos;s some evidence, he said, that minimizing pulsatile stimulation may delay the onset of dyskinesias.
              &lt;p&gt; 
              &lt;p&gt;Because entacapone -- which prolongs the half-life of levodopa by inhibiting the enzyme COMT (catechol o-methyl transferase) -- is approved to reduce loss of motor function in late Parkinson&apos;s, Dr. Olanow and colleagues decided to test its use against development of dyskinesias in early disease.
              &lt;p&gt; 
              &lt;p&gt;In their study, 745 patients who required initiation of levodopa were randomized to receive either levodopa/carbidopa (LC) or levodopa/carbidopa/entacapone (LCE). (Carbidopa is dosed with levodopa to reduce nausea.)
              &lt;p&gt; 
              &lt;p&gt;Treatment continued for at least 134 weeks. The main outcome measure was time to onset of dyskinesias.
              &lt;p&gt; 
              &lt;p&gt;Dyskinesias occurred earlier in patients receiving the entacapone combination than in those receiving LC, with 42% of the entacapone patients developing them after a mean of 74 weeks compared with 32% developing them after a mean of 79 weeks in the LC group (hazard ratio 1.29, &lt;em&gt;P&lt;/em&gt;=0.038).
              &lt;p&gt; 
              &lt;p&gt;Dr. Olanow suggested that the unexpected results might by explained by differences in total levodopa exposure between the two groups.
              &lt;p&gt; 
              &lt;p&gt;Pharmacokinetic analysis showed that patients receiving the entacapone combination received significantly greater levodopa dose equivalents because of the larger area under the curve.
              &lt;p&gt; 
              &lt;p&gt;&quot;This likely accounted for these results,&quot; Dr. Olanow said.
              &lt;p&gt; 
              &lt;p&gt;&quot;There is no reason to begin entacapone in early Parkinson&apos;s disease,&quot; he said, in an attempt to delay dyskinesias. He noted that these results do not weaken the rationale for its use later in the disease.
              &lt;p&gt; 
              &lt;p&gt; 
              &lt;p&gt;&lt;table cellspacing=&quot;0&quot; hspace=&quot;1&quot; style=&quot;border-style:solid; border-width:1px; border-color:#8dabbc; font-family:arial; font-size:12px; background-color:#DBE9F2; padding:5px 5px 5px 5px;&quot;&gt;
&lt;tr&gt;&lt;td&gt;The study was funded by Novartis Pharma AG and Orion Pharma.
              &lt;p&gt;Dr. Olanow has served as a consultant for Teva Neuroscience, Novartis, and Boehringer Ingelheim and has been a member of the Scientific Advisory Board for Teva Neuroscience, Novartis, Boehringer Ingelheim, and Ceregene.&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
            
    </recommendedItem>
    <recommendedItem id="20090101_19_1881"
                     title="ICPDMD: Adjunct Safinamide Improves Advanced Parkinson&apos;s Disease"
                     score="-0.005"
                     href="http://www.medpagetoday.com/Neurology/ParkinsonsDisease/tb/14673?impressionId=1265746168761"
                     
      PARIS, June 12 -- The investigational drug safinamide improves &quot;on&quot; time in advanced Parkinson&apos;s disease without an increase in troublesome dyskinesias, researchers here said.
        &lt;p&gt;
        &lt;p&gt;Compared with placebo, low-dose safinamide provided 0.5 hours additional &quot;on&quot; time daily, while high-dose safinamide provided 0.7 hours more than placebo (&lt;em&gt;P&lt;/em&gt;=0.007), Rupam Borgohain, M.D., of Nizam&apos;s Institute of Medical Sciences in Hyderabad, India, reported at the International Congress of Parkinson&apos;s Disease and Movement Disorders meeting.
        &lt;p&gt;
          &lt;p&gt;&quot;Safinamide provides an extra half hour of &apos;on&apos;  time to patients who have maxed out their other treatment options,&quot; he said.
        &lt;p&gt;
          &lt;p&gt;Patients with advanced Parkinson&apos;s disease typically develop motor complications, including a reduction in &quot;on&quot; time (time spent responsive to levodopa). They also develop dyskinesias. Several adjunct medications provide some benefit, but patients are often left with residual &quot;off&quot; time, Dr. Borgohain said.
        &lt;p&gt;
          &lt;p&gt;Safinamide is a novel drug with a dual mechanism: it enhances dopaminergic activity through inhibiting monoamine oxidase B-catalyzed dopamine breakdown, and reduces overactivity of glutamatergic signaling by inhibiting glutamate release.
        &lt;p&gt;
          &lt;p&gt;The latter function is important, Dr. Borgohain said, because it is thought this system may be responsible for development of dyskinesias.
        &lt;p&gt;
          &lt;p&gt;Safinamide has been tested successfully in early Parkinson&apos;s disease. To test its efficacy in advanced cases, researchers enrolled 669 patients, average age 60, with disease duration of eight years. They had approximately five hours of daily &quot;off&quot; time despite taking levodopa and one or more adjunct medications.
        &lt;p&gt;
          &lt;p&gt;Patients received placebo or one of two doses of safinamide. They were assessed over 24 weeks by a daily diary of &quot;on&quot; time without dyskinesias or with only minor dyskinesias (the primary efficacy variable).
        &lt;p&gt;
          &lt;p&gt;Other assessments included the Unified Parkinson&apos;s Disease Rating Scale (UPDRS), Hamilton Depression Scale, and Dyskinesia Rating Scale.
        &lt;p&gt;
          &lt;p&gt;Total daily &quot;on&quot; time increased by 1.0 hours for patients receiving placebo, by 1.5 hours for those on low-dose safinamide (&lt;em&gt;P&lt;/em&gt;=0.0082 versus placebo), and by 1.6 hours for those on high-dose safinamide (&lt;em&gt;P&lt;/em&gt;=0.0048 versus placebo).
        &lt;p&gt;
          &lt;p&gt;Neither &quot;on&quot; time with minor dyskinesias, &quot;on&quot; time with troublesome dyskinesias, nor time asleep was significantly different between groups.
        &lt;p&gt;
          &lt;p&gt;Treatment also improved the UPDRS score versus placebo. There was no change in dyskinesias in any group. 
        &lt;p&gt;
          &lt;p&gt;Depression improved from safinamide treatment as well, although only in the higher-dose group. Those patients experienced a 1.0-point improvement in the Hamilton score, versus 0.3 points for the placebo-treated patients (&lt;em&gt;P&lt;/em&gt;=0.018).
        &lt;p&gt;
          &lt;p&gt;This effect on depression, Dr. Borgohain said, is potentially important for this type of patient. Patients with moderate depression were excluded from the study, he noted, but mild depression is quite common in advanced Parkinson&apos;s disease.
        &lt;p&gt;
          &lt;p&gt;The only emergent adverse effect affecting safinamide-treated patients more than placebo-treated patients were dyskinesias, but these were mild and nontroublesome.
        &lt;p&gt;
          &lt;p&gt;There were six deaths during the study -- two in the placebo group, two in the low-dose safinamide group not attributable to treatment, and two in the same group of unknown cause.
        &lt;p&gt;
          &lt;p&gt;Based on the results of this study, Dr. Borgohain said, &quot;Safinamide may be a valuable adjunct to levodopa treatment in more advanced Parkinson&apos;s disease patients.&quot;
        &lt;p&gt;
          &lt;p&gt;&lt;table cellspacing=&quot;0&quot; hspace=&quot;1&quot; style=&quot;border-style:solid; border-width:1px; border-color:#8dabbc; font-family:arial; font-size:12px; background-color:#DBE9F2; padding:5px 5px 5px 5px;&quot;&gt;
&lt;tr&gt;&lt;td&gt;Dr. Borgohain disclosed no financial conflicts of interest.
          &lt;p&gt;The study was funded by Newron and Merck Serono.&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
         
    </recommendedItem>
</recommendedContent>