***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background : Patients with Parkinson disease ( PD ) may present with various types of pain . In some instances , no cause can be identified and pain is considered a primary disorder ( primary central pain [ PCP ] ) . We hypothesized that PCP in patients with PD ( PD-PCP ) may be due to a dysfunction of pain pathways or the processing of pain inputs in the CNS . Methods : We carried out a psychophysical and neurophysiologic study in 9 patients with PD-PCP , 9 patients with PD without pain ( PD-NoP ) , and 9 healthy control subjects . We assessed the clinical characteristics of pain , performed quantitative sensory testing with thermal probes , and recorded laser-evoked potentials ( LEPs ) and laser-induced sudomotor skin responses ( l-SSRs )  in “ off ” and “ on ” conditions . Results : In “ off ” condition , patients with PD-PCP had lower heat pain and laser pinprick thresholds , higher LEP amplitudes , and less habituation of the l-SSR in comparison with PD-NoP patients and control subjects . Abnormalities were more marked in the most affected side . In “ on ” condition , psychophysical and neurophysiologic differences disappeared or were significantly attenuated . Conclusion : Conduction along peripheral and central pain pathways is normal in patients with Parkinson disease with or without primary central pain . However , apart from signs of hyperalgesia , our patients exhibited lack of habituation of sympathetic sudomotor responses to repetitive pain stimuli , suggesting an abnormal control of the effects of pain inputs on autonomic centers . Abnormalities were attenuated by l-dopa , suggesting that the dysfunction may occur in dopamine-dependent centers regulating both autonomic function and inhibitory modulation of pain inputs To examine the effects of levodopa ( L-dopa ) and deep brain stimulation of the subthalamic nucleus ( STN-DBS ) on sensory symptoms and signs in Parkinson 's disease ( PD ) . Seventeen patients with PD were included . ( 1 ) Presence of sensory symptoms and ( 2 ) effects of L-dopa and STN-DBS on sensory symptoms and signs [ assessed by quantitative sensory testing ( QST ) ] were examined 6 months after starting STN-DBS . In addition , in 12 of these patients , presence of sensory symptoms prior and post STN-DBS was compared . Pain was most frequently nociceptive . In about 30 - 40 % , pain and sensory symptoms were associated with PD motor symptoms . In most of these cases , pain responded to L-dopa .  Intensity of pain was reduced post STN-DBS compared to pre STN-DBS . L-Dopa had no influence on detection thresholds , whereas STN-DBS improved thermal detection thresholds . However , thermal and mechanical pain thresholds were uninfluenced by L-dopa or STN-DBS . Although some patients reported an improvement of pain with STN-DBS or L-dopa , objective ly pain sensitivity as assessed by QST was not altered by STN-DBS or L-dopa suggesting that there is no evidence for a direct modulation of central pain processing by L-dopa or STN-DBS Plastic changes within the striatum result ing from pulsatile dopaminergic stimulation are thought to lead to dyskinesia in patients with Parkinson 's disease ( PD ) . The basal ganglia play a role in processing pain . We hypothesized that the plastic changes that lead to dyskinesia may also mediate pain responses . Our objective was to compare the change in pain sensitivity after levodopa administration between stable responders , fluctuators without dyskinesia , and dyskinetic patients , and to compare pain sensitivity between PD and healthy subjects . Fifty patients with PD were assessed with cold water immersion after overnight withdrawal of dopaminergic medications and again after a st and ard levodopa challenge , and carefully classified into stable responder ( n = 12 ) , fluctuator ( n = 15 ) , and dyskinetic ( n = 23 ) groups . Twenty age-matched controls were also tested . PD patients " off"-medication had a lower threshold ( P = 0.016 ) and tolerance ( P < 0.0001 ) to cold pain compared to controls . After levodopa administration , dyskinetic patients experienced a large increase in cold pain threshold ( 48 % ) and tolerance ( 66 % ) that was absent in stable responders ( P = 0.038 and P = 0.015 ) ; there was no significant difference in pain sensitivity change scores between the fluctuator and either the stable responder or dyskinetic groups . Our results suggest that dyskinesia and pain may share common pathophysiological mechanisms in PD Background : Patients suffering from Parkinson ’s disease ( PD ) describe painful sensations that could be related to neuropathic pain . Experimental data have indicated the involvement of basal ganglia and dopaminergic pathways in central nociceptive processing . Aim : The objective of this study was to assess and compare the effect of levodopa on the objective pain threshold in patients with PD and healthy subjects . Methods : The objective pain threshold was assessed by the nociceptive flexion reflex ( RIII ) in 13 PD patients and 10 healthy subjects . Patients and healthy subjects were evaluated under two r and omised conditions : with levodopa ( ON ) and without ( OFF ) . Results : Levodopa significantly increased the RIII threshold of PD patients ( 6.9 ( 1.2 ) mA in the OFF condition vs 8 ( 1.1 ) mA in the ON position ; p = 0.02 ) . RIII threshold was significantly lower in PD patients than in healthy subjects in the OFF condition ( 6.9 ( 1.2 ) mA vs 9.7 ( 3.4 ) mA ; p = 0.02 ) . RIII threshold did not change after levodopa administration in healthy subjects . Conclusion : These results provide evidence of a dopaminergic modulation of objective pain threshold in PD patients . In addition , the decrease in RIII threshold in PD patients , in the OFF condition , compared with controls , confirms the existence of an objective pain perception disturbance in PD BACKGROUND Patients suffering from Parkinson 's disease ( PD ) frequently experience painful sensations that may be due to central modification of nociception in PD . We compared pain thresholds and cerebral activity in nociceptive areas using Positron Emission Tomography ( PET ) during nociceptive stimulation before ( OFF condition ) and after ( ON condition ) levodopa challenge between nine PD patients with and nine PD patients without neuropathic pain . METHODS Pain thresholds were determined using a cold pressor test in the two conditions . We used H2(15)O PET to study the regional cerebral blood flow changes in subjects while they received  alternate r and omized noxious and innocuous cold stimuli during OFF and ON periods . RESULTS Pain thresholds were not significantly different between PD patients with and without pain in either condition ( OFF and ON ) . In both groups of PD patients , levodopa significantly raised pain threshold ( F1,16 = 26.71 ; p < 0.0001 ) with a mean variation of -2.7 ( ±2.3 ° C ) . In the OFF condition , PD patients with pain had a lower pain activation in the right prefrontal cortex and posterior insula and a higher pain activation in the right anterior cingulate cortex ( BA32/8 ) than pain-free patients . Levodopa significantly reduced pain-induced-activation in the right insula and in the anterior cingulate cortex in both groups . CONCLUSION Levodopa decreased nociceptive perception in both PD patients with and without pain . In PD patients with neuropathic pain the medial affective pathway was preferentially recruited whereas pain-free PD patients exhibited a greater activation in lateral discriminative nociceptive areas INTRODUCTION Trigemino-cervical-spinal reflexes ( TCSRs ) are complex brainstem stereotyped nociceptive responses involved in a defensive withdrawal reaction of the head from facial nociceptive stimuli . OBJECTIVE The present study was undertaken to collect data on possible TCSR abnormalities in idiopathic Parkinson 's disease ( PD ) and investigate any correlation with motor signs and L-DOPA administration . METHODS TCSRs were registered from the semispinalis capitis and biceps brachii muscles after electrical stimulation of the supraorbital nerve in 18 patients with PD and 24 controls . The latency ( L ) and area ( A ) , as well as the sensory ( ST ) , painful ( PT ) and reflex ( RT ) thresholds were measured during the ' off ' and ' on ' state , and possible correlations with the UPDRS III total score , selected subscores ( tremor , neck rigidity , upper limb rigidity , akinesia , rising from a chair , posture and posture instability ) and duration of illness were investigated . RESULTS Significant changes between controls and PD patients were found in the L , A , PT and RT of TCSRs . These results were not significantly influenced by L-DOPA treatment . A significant correlation was found between neck rigidity , postural instability scores and duration of illness and the TCSR L and A values in PD patients in the ' off ' state . CONCLUSIONS TCSRs abnormalities , combined with dopamine resistance , are consistent with a primary loss of brainstem neurons mediating a complex sensory-motor integration including neck muscle tone and postural control as well as the head withdrawal reaction to the nociceptive stimuli . SIGNIFICANCE TCSRs may represent a useful tool for the assessment of brainstem sensory-motor function in PD as well as other movement and degenerative disorders OBJECTIVE To assess levodopa dose effect on pain thresholds in Parkinson 's disease ( PD ) patients using an experimental nociceptive thermal stimulation . PATIENTS AND METHODS We evaluated pain thresholds in 20 PD patients treated by dopaminergic drugs .  We assessed heat and cold pain thresholds by using 2 different methods ( method of limits and method of levels ) , intensity-response curve and tolerance threshold . Each PD patient was evaluated in two conditions : ON ( after administration of leovdopa and OFF ( after acute levodopa withdrawal ) . The order was r and omized . RESULTS The mean age of patients was 652+/-9.9 years and the mean duration was 9.3+/-3.3 years .  Heat pain thresholds were statistically higher in ON versus OFF condition using both methods ( 44.1+/-3,6 degrees C versus 42.3+/-3,1 degrees C , method of levels , p=0.02 ) . Cold pain thresholds were statistically higher in ON versus OFF condition only using method of levels ( 17.9+/-4,4 degrees C versus 19.6+/-4,2 degrees C , p=0.02 ) . Heat pain tolerance was statistically higher in ON versus OFF condition ( 21.4+/-21.6 seconds versus 14.7+/-20.3 seconds , p=0.02 ) . CONCLUSION This study showed that levodopa increased heat and cold pain thresholds and heat pain tolrance in PD patients . This suggests that dopaminergic drugs could have an analgesic effects on PD related pain Patients suffering from Parkinson 's disease ( PD ) frequently experienced painful sensations that could be in part due to central modification of nociception . We compared pain threshold before and after administration of levodopa in PD patients and in controls , and investigated cerebral activity with positron emission tomography ( PET ) during experimental nociceptive stimulation . Pain threshold was determined using thermal stimulation during two r and omized conditions : off and on . We performed H(2 ) (15)O PET analysis of regional cerebral blood flow on subjects while they received alternate r and omized noxious and innocuous stimuli during off and on conditions . In off condition , pain threshold  in nine PD patients was significantly lower than in nine controls . Administration of levodopa significantly raised pain threshold in PD patients but not in controls . During off condition , there was a significant increase in pain-induced activation in right insula and prefrontal and left anterior cingulate cortices in PD compared to control group . Levodopa significantly reduced pain-induced activation in these areas in PD . This study shows that pain threshold is lower in PD patients but returns to normal ranges after levodopa administration . Moreover , PD patients have higher pain-induced activation in nociceptive pathways , which can be reduced by levodopa Patients with Parkinson 's disease ( PD ) frequently experience pain that could be in part due to central modification of nociception . In this r and omized controlled double blind study , we compared the effect of apomorphine versus placebo on pain thresholds and pain-induced cerebral activity in 25 patients with PD .  Subjective pain threshold ( using thermal stimulation , thermotest ) , objective pain threshold ( nociceptive flexion reflex ) , and cerebral activity ( H(2)(15)O PET ) during noxious and innocuous stimulations were performed . Neither subjective nor objective pain thresholds nor pain activation profile were modified by apomorphine compared with placebo in 25 PD patients .  Apomorphine has no effect on pain processing in PD . We suggest that other monoamine systems than dopaminergic system could be involved Objective : To investigate the acute effect of subthalamic nuclei deep brain stimulation ( STN-DBS ) and levodopa on pain and tolerance thresholds in patients with Parkinson disease . We hypothesized that a modification of pain threshold after STN-DBS would suggest a central modification of pain perception , whereas the absence of pain threshold change after STN-DBS would correspond to a peripheral mechanism via a decrease of painful stimuli . Methods : Nineteen patients with Parkinson disease were included in this double-blind , r and omized , crossover study . Postoperatively , we 
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Results were much more heterogenous when PD patients on medications were compared with HC off medications , with most trials reporting no significant difference in pain thresholds between groups .
No significant differences were found in pain thresholds for trials that compared PD patients on medications and HC on medications .
PD patients are more sensitive to noxious stimuli compared to HC when tested in the off medication state .
This increase in pain sensitivity is observed across all modalities , but is not as apparent when PD patients are administered Levodopa , suggesting that dopamine deficient states may contribute to hyperalgesia .
However , it remains to be seen whether or not increased pain sensitivity translates clinical ly into increased prevalence of pain .
Similarly , it is unclear if dopaminergic medications influence pain sensitivity .