Effects Of Antiparkinsonian Medication Research Articles

Medication adversely impacts visually-guided eye movements in Parkinson’s disease

ObjectiveWe examined whether previous inconsistent findings about the effect of anti-Parkinsonian medication on visually-guided saccades (VGS) were due to the use of different paradigms, which change the timing of fixation offset and target onset, or different target eccentricities. MethodsThirty-three participants with Parkinson’s disease (PD) completed the VGS tasks OFF and ON medication, along with 13 healthy controls. Performance on 3 paradigms (gap, step, and overlap) and 2 target eccentricities was recorded. We used mixed models to determine the effect of medication, paradigm, and target eccentricity on saccade latency, gain, and peak velocity. ResultsFirst, we confirmed known paradigm effects on latency, and target eccentricity effects on gain and peak velocity in participants with PD. Second, latency was positively associated with OFF medication Movement Disorders Society – Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) motor score in PD. Third, medication prolonged latency for the larger target eccentricity across the 3 paradigms, while decreasing gain and peak velocity in the step paradigm across target eccentricities. ConclusionsMedication adversely affected and was not therapeutically beneficial for VGS. Previous inconsistencies may have resulted from chosen target eccentricity. SignificanceThe negative medication effect on VGS may be clinically significant, as many activities in daily life require oculomotor control, inhibitory control, and visually-guided shifts of attention.

Visuomotor control in patients with Parkinson's disease

Previous studies have suggested that the deteriorated visuomotor control in patients with PD (Parkinson's disease) is due to deficits in various aspects of the sensory-motor processing rather than motor control itself. In the current study, by taking a control-theoretic approach, we systematically examined how PD and antiparkinsonian medication affect visuomotor control and the underlying sensory-motor system.We tested 20 PD patients in both ON and OFF medication states and 20 demographically matched healthy controls with a commonly used manual control task. Specifically, in each 95-s trial, participants were instructed to use a joystick to control a randomly moving target to keep it centered on a computer display. We found that although antiparkinsonian medication improved visuomotor control in PD patients, they still showed significantly decreased control precision (measured by RMS error) and response amplitude (gain) as well as increased response delay (phase lag) compared with healthy controls.Our model-driven analysis revealed that PD impairs the responsiveness and the predicting ability of the sensory–motor system as well as the stability of the neuromuscular system. Taking antiparkinsonian medication improves the responsiveness of the sensory–motor system. More importantly, it improves the ability of the sensory–motor system to make sensory predictions of the current control actions (see Wolpert et al., 1995) to anticipate the input error signals and generate control responses ahead of time up to the level of healthy controls. However, taking antiparkinsonian medication does not improve the stability of the neuromuscular system. These results support the claim that the effect of antiparkinsonian medication on visuomotor control is mainly through improving visual-stimulus-dependent sensory–motor processing.The present study provides the first quantitative examination of the effects of PD and antiparkinsonian medication on the visual-stimulus-dependent sensory–motor and visual-stimulus-independent neuromuscular systems underlying visuomotor control. The findings have practical implications for developing sensitive assessment tools to evaluate the efficacy of different therapies for PD and preliminary screening and training tools for fitness-to-drive in PD patients.

Effect of Anti-parkinsonian Medications on Gait and Balance in Individuals with Parkinson's Disease

Anti-parkinsonian medications can improve gait and balance in individuals with idiopathic Parkinson's disease (PD) who display the postural instability gait deficit type of Parkinson's. PURPOSE: The purpose of this study was to compare temporal and spatial characteristics of gait and the limits of stability postural test while on and off medications. METHODS: Eleven individuals with PD who had a history of falls and gait and balance deficits were recruited. The subjects were tested with a computerized gait mat during usual and fastest walking conditions. Computerized posturography was used to test the limits of stability for each subject. The subjects arrived at the laboratory without taking the first dosage of their medications, the "off" medication condition. Each of the tests was completed for the off condition. Subjects then took their medications and waited for 45 minutes to an hour prior to being retested while "on" medications. RESULTS: The subjects were mean age 74±9 years, BMI 26±4.7, 6.2±6.0 years since diagnosis, and 2.7±0.5 on the Hoehn &Yahr Disability Scale. Usual walking velocity was 81.5±12.9 cm/s off and 87.6±21.3 cm/s on, and the fastest velocity was 118.9±26.5 cm/s off and 116.5±30.5 cm/s on. Usual cadence decreased significantly from off to on (121.4± 15.5 steps/min vs. 113.6± 13.9 steps/min), but increased for the fastest walk (136.9± 20.8 steps/min off vs. 147.8 ± 23.4 steps/min on. Step length usual speed increased from 41.0 cm±8.9 off vs. 45.9±8.2 cm on, but decreased during fastest walking from 51.7±8.6 cm off to 47.8±10.6 cm on. For the limits of stability test, reaction time forward increased from off to on (1.5±0.7 s off vs. 1.1 ±0.3 s on, but was relatively unchanged for backward movements (1.3±0.4 s off vs. 1.2±0.5 s on). Movement velocity showed a small change off vs. on for forward (2.1±0.8 °/s off vs. 2.2±0.6 °/s on) and backward movements (1.8±1.0 °/s off vs. 1.9± 0.7 °/s on).Maximum excursion increased while on for forward targets (60.3±20.1 % off vs. 69.0±9.9 % on) and backward targets (50.8±18.0 % off vs. 58.8±15.5 % on). CONCLUSIONS: Anti-parkinsonian medications have a variable impact on the temporal and spatial parameters of gait and limits of stability balance measures. This suggests that other interventions should be explored to improve gait and balance.

The Role of Telephone Counseling in Management of Parkinson’s Disease Patients

Background: Various nonpharmacologic managements are important fundamental elements in the treatment of Parkinson’s disease (PD). W e aimed to investigate the role of telephone counseling in managing PD patients. Methods: From November 2006 to January 2007, we studied 243 PD patients at outpatient clinic of Asan Medical Center. Detailed telephone counseling was provided using a list structured questionnaires. Results: There were 73 men and 170 women with an age range of 17 to 85 years (mean age, 64.9 years). Mean age at onset was 59.5 years (range, 14-82 years) and mean disease duration was 5.6 years (range, 0.3-25 years). The contents of telephone counseling included adverse effects of anti-Parkinso nian medications (24.4%), aggravation of motor symptoms (18.7%) , problems due to comorbi dities (17.8%) , how to take medi cine (1 3.6%), activities of daily living (diet, bowel, sleeping and safety) (12.6%), complementary or alternative medicines (3.9%) and knowledge about PD (3.0%). Persons who responded to use the telephone counseling included patients (37.9%), offspring (36.2%), spouses (17.7%) and other relatives (7.4%). Persons who received the telephone counseling were determined by level of education, sex, cohabitation and Hoehn-Yahr stage. Contents of telephone counseling varied significantly with Hoehn-Yahr stage and persons who used the telephone counseling. Conclusions: Our results suggest that support system with telephone counseling may provide beneficial therapeutic intervention in PD patients, especially for those with advanced PD. The most cost-effective method for telephone support needs to be studied.

Chronic delusional hallucinatory psychosis in early-onset Parkinson's disease: drug-induced complication or sign of an idiopathic psychiatric illness?

Chronic delusional psychosis with hallucinations (CDHP) is commonly assumed to complicate the later stages of Parkinson's disease, as a side effect of antiparkinsonian medication. We studied 7 patients with early onset PD, who had developed psychiatric manifestations consisting in CDHP after a few years of antiparkinsonian therapy. All patients underwent a neurological, psychiatric and brain imaging (CT or MRI) evaluation. Detailed clinical history was recorded in order to reveal prior psychiatric illness and to analyse the relationship between neurological disease, cognitive impairment and psychosis. Our findings suggest that CDHP occurring in patients with early onset PD, normal or slightly impaired cognitive functions and normal CT/MRI scans is invariably the expression of a coexisting psychiatric illness which prior to onset of the neurologic disease had not been correctly diagnosed and which has been disclosed by dopaminergic therapy.

Neuropsychiatric Aspects of Parkinson’s Disease

Parkinson's disease (PD), a disorder characterized by movement abnormalities, is frequently complicated by psychiatric syndromes. Psychiatric assessment of the PD patient requires familiarity with the motor and cognitive aspects of PD, the various effects of antiparkinsonian medications, and how these relate to mental status changes and psychiatric phenomena. This review describes the various motor and nonmotor features of PD and focuses on the differential diagnosis of affective disorders in PD and their treatment.

Anxiety disorders in Parkinson's disease

Clinically significant anxiety syndromes are a common problem in PD, with prevalence rates of up to 40% of patients with Parkinson's disease (PD). Although limited attention has been paid to PD-related anxiety disorders, they contribute substantially to morbidity and caregiver burden. In some patients, the anxiety syndrome is a prevailing problem, over and above the impairment related to motor dysfunction. There is also evidence that anxiety disorders in PD are fundamentally related to underlying neurodegenerative processes. While anxiety syndromes occur in isolation, there is also overlap among anxiety symptoms and signs, PD-related depressive syndromes, PD motor phenomena, and effects of antiparkinsonian medications. Together, these factors can contribute to the misattribution of pathological anxiety as a normal psychological reaction to motor-related disability, and, hence, reduced recognition and treatment of a discrete anxiety syndrome. The primary aims of this article are to review the clinical features of the different anxiety syndromes in PD, describe the potential interplay between motor, cognitive, and affective abnormalities, and discuss the proposed mechanisms of anxiety disorders in PD and related treatment approaches.

Gastrointestinal motility problems in patients with Parkinson's disease. Effects of antiparkinsonian treatment and guidelines for management.

Gastrointestinal (GI) motility disorders are frequent in patients with Parkinson's disease, manifesting mainly as dysphagia, disorders of gastric emptying and constipation. The most likely causes of these disorders are cerebral degeneration and degeneration of the myenteric plexus. Although the effect of antiparkinsonian medication is largely overestimated, it certainly has an influence and should be adapted accordingly in patients with GI motility disorders. In particular, anticholinergic drugs should be avoided, and anamnesis, clinical examination and, if necessary, diagnostic tests performed. Domperidone, a peripheral dopamine antagonist, is the drug of choice for motility disorders of the upper GI tract, although cisapride is an alternative. In the lower GI tract, conservative therapeutic options should be used in the first instance. The administration of cisapride leads to a marked temporary improvement in symptoms in lower GI disorders, while rare forms of anism (involuntary dystonic contraction of the anal sphincter) may be treated with botulinum toxin.

Adrenal medulla and Parkinson's disease

Parkinson's disease has been described as a multisystem disorder that includes alterations in the function of the autonomic nervous system. The activity of the adrenal medulla in this disease has not been thoroughly investigated. Previous reports are reviewed that demonstrate that the adrenal medullae of parkinsonian patients are compromised, having a decreased content of all catecholamines and several neuropeptides. An animal model was used to investigate whether the observations made in human patients were related to extended treatment with antiparkinsonian medications or were a natural concomitant of the disease. Administration of L-dopa and/or carbidopa to C57BL mice for 4-16 weeks had no significant effect on the level of any of the adrenal medullary catecholamines. Treatment with MPTP 4-16 weeks prior to sacrifice did not deplete adrenal medullary catecholamines in these animals, thus not fully mimicking Parkinson's disease in this animal model. The only significant effect was an interaction between group (MPTP or control) and treatment with antiparkinsonian medications; L-dopa, in the absence and presence of carbidopa, had opposite effects in the two groups. Based primarily on the lack of effect of antiparkinsonian medications on adrenal medullary catecholamines, it was concluded that the adrenal medullary depletion observed in human patients was a peripheral concomitant of Parkinson's disease.

The rabbit syndrome and antiparkinsonian medication in schizophrenic patients.

Effects of antiparkinsonian medication on the rabbit syndrome (RS) and accompanying parkinsonian symptoms were studied in 5 schizophrenic inpatients receiving long-term antipsychotic medication. All patients showed early improvement of RS following additional treatment with trihexyphenidyl or biperiden, with a significant reduction in the RS score also observed. The improvement of RS paralleled improvement of the parkinsonian symptoms, with the score of the Simpson-Angus rating scale significantly reduced. Our data provide further evidence that the underlying mechanism of RS is similar to that of acute forms of drug-induced parkinsonism.