Importance Parkinson disease is the second most common neurodegenerative disease worldwide. Although no available therapies alter the underlying neurodegenerative process, symptomatic therapies can improve patient quality of life. Objective To provide an evidence-based review of the initial pharmacological management of the classic motor symptoms of Parkinson disease; describe management of medication-related motor complications (such as motor fluctuations and dyskinesia), and other medication adverse effects (nausea, psychosis, and impulse control disorders and related behaviors); and discuss the management of selected nonmotor symptoms of Parkinson disease, including rapid eye movement sleep behavior disorder, cognitive impairment, depression, orthostatic hypotension, and sialorrhea. Evidence Review References were identified using searches of PubMed between January 1985 and February 2014 for English-language human studies and the full database of the Cochrane Library. The classification of studies by quality (classes I-IV) was assessed using the levels of evidence guidelines from the American Academy of Neurology and the highest-quality data for each topic. Results Although levodopa is the most effective medication available for treating the motor symptoms of Parkinson disease, in certain instances (eg, mild symptoms, tremor as the only or most prominent symptom, aged Conclusions and Relevance Strong evidence supports using levodopa and dopamine agonists for motor symptoms at all stages of Parkinson disease. Dopamine agonists and drugs that block dopamine metabolism are effective for motor fluctuations and clozapine is effective for hallucinations. Cholinesterase inhibitors may improve symptoms of dementia and antidepressants and pramipexole may improve depression. Evidence supporting other therapies for motor and nonmotor features is less well established.

https://jamanetwork.com/HttpHandlers/ArticlePdfHandler.ashx?journal=JAMA&articleId=1861807&pdfFileName=jrv140005.pdf

Pharmacological Treatment of Parkinson Disease: A Review

European Organization for Research and Treatment of Cancer

The Movement Disorder Society (MDS) Task Force on Evidence-Based Medicine (EBM) Review of Treatments for Parkinson's Disease (PD) was first published in 2002 and was updated in 2005 to cover clinical trial data up to January 2004 with the focus on motor symptoms of PD. In this revised version the MDS task force decided it was necessary to extend the review to non-motor symptoms. The objective of this work was to update previous EBM reviews on treat- ments for PD with a focus on non-motor symptoms. Level-I (randomized controlled trial, RCT) reports of pharmacological and nonpharmacological interventions for the non-motor symptoms of PD, published as full

/pdf/the-movement-disorder-society-evidence-based-medicine-review-2fyuhos0nl.pdf

The Movement Disorder Society Evidence-Based Medicine Review Update: Treatments for the non-motor symptoms of Parkinson's disease

Parkinson disease (PD) is an age-related neurodegenerative disorder that affects as many as 1-2% of persons aged 60 years and older. With the aging of the population, the frequency of PD is expected to increase dramatically in the coming decades. Current therapy is largely based on a dopamine replacement strategy, primarily using the dopamine precursor levodopa. However, chronic treatment is associated with the development of motor complications, and the disease is inexorably progressive. Further, advancing disease is associated with the emergence of features such as freezing, falling, and dementia which are not adequately controlled with dopaminergic therapies. Indeed, it is now appreciated that these nondopaminergic features are common and the major source of disability for patients with advanced disease. Many different therapeutic agents and treatment strategies have been evaluated over the past several years to try and address these unmet medical needs, and many promising approaches are currently being tested in the laboratory and in the clinic. As a result, there are now many new therapies and strategic approaches available for the treatment of the different stages of PD, with which the treating physician must be familiar in order to provide patients with optimal care. This monograph provides an overview of the management of PD patients, with an emphasis on pathophysiology, and the results of recent clinical trials. It is intended to provide physicians with an understanding of the different treatment options that are available for managing the different stages of the disease and the scientific rationale of the different approaches.

The scientific and clinical basis for the treatment of Parkinson disease (2009)

Background: The Ashworth Scale and the modified Ashworth Scale are the primary clinical measures of spasticity. A prerequisite for using any scale is a knowledge of its characteristics and limitations, as these will play a part in analysing and interpreting the data. Despite the current emphasis on treating spasticity, clinicians rarely measure it.Objectives: To determine the validity and the reliability of the Ashworth and modified Ashworth Scales.Study design: A theoretical analysis following a structured literature review (key words: Ashworth; Spasticity; Measurement) of 40 papers selected from the BIDS-EMBASE, First Search and Medline databases.Conclusions: The application of both scales would suggest that confusion exists on their characteristics and limitations as measures of spasticity. Resistance to passive movement is a complex measure that will be influenced by many factors, only one of which could be spasticity. The Ashworth Scale (AS) can be used as an ordinal level measure of resistance to pa...

A review of the properties and limitations of the Ashworth and modified Ashworth Scales as measures of spasticity

To investigate the safety and efficacy of botulinum toxin type A (BoNTX) treatment to reduce sialorrhea in Parkinson's disease (PD), a double-blind, randomized, placebo-controlled study enrolled 32 PD patients complaining of excessive drooling. Patients received either 50 U Botox in each parotid gland or placebo without using ultrasound guidance. Subjects treated with BoNTX experienced a reduction in both drooling frequency and familial and social disability (Time × Group effect: P < 0.01), as well as in saliva production (Time × Group effect: P < 0.0001). No adverse events were recorded. BoNTX injections are safe and effective treatment for the management of PD-related drooling. © 2006 Movement Disorder Society

Botulinum toxin type A for drooling in Parkinson's disease: a double-blind, randomized, placebo-controlled study.

Objective: Although the botulinum toxin A (BTX-A) treatment has proved effective in spasticity management, no information is available with regard to the effects of repeated injections over time. Design: To evaluate the effects of BTX-A on moderate or severe upper limb spasticity, an exploratory investigation was performed on 28 stroke patients treated for 2 yr or longer and observed for 3 yr. Every 3 to 5 mo, each patient received BTX-A injections in upper limb muscles. The assessment, performed before and 1 mo after each injection for a median of 28 mo, included technical and functional objectives and the burden of care. The former were evaluated by using the modified Ashworth Scale for spasticity and the goniometric measurement of rest position and range of motion; functional objectives were evaluated by means of the Frenchay Arm Test and a patient/caregiver goals assessment scale. Results: BTX-A treatment was followed by an improvement in all technical outcome measures. Motor dexterity scores improved in only 8 of 28 patients, VS. daily living activities, which increased in all subjects. Although the average dosage injected per session did not change, intervals between injections became longer. No relationship between either spasticity onset or residual motoricity and response to treatment could be found. Conclusions: This investigation is relevant clinically because repeated BTX-A injections show unchanging effectiveness in the management of focal spasticity after stroke.

Post-stroke spasticity management with repeated botulinum toxin injections in the upper limb.

To investigate the safety, efficacy and effectiveness of botulinum toxin type-B (BTX-B) injections into the parotid glands to reduce drooling in Parkinson’s disease (PD) subjects A double-blind, randomised, placebo-controlled study enrolled 36 advanced phase PD subjects who complained of disabling drooling Patients received either 4000U BTX-B or placebo Anatomically guided injections were performed Outcome measures were chosen to assess both the subjective feeling of improvement (i e the Drooling Severity and Frequency Scale, DSFS, visuo-analogic ratings of familial distress, VAS-FD, and social distress, VAS-SD) and objective saliva reduction (saliva production over five minutes was checked by weighing dental rolls) The Global Impression Score (GIS) was also applied, rating improvement from 0 to 3 One month after injections, BTX-B patients showed a meaningful improvement in almost all subjective outcomes Two-way analysis of variance gave a significant time × treatment effect, F-value being 525 (p < 00001) for DS-FS, 232 (p < 00001) for VAS-FD, 29 (p < 00001) for VAS-SD, and 289 (p < 00001) for UPDRSADL drooling item score All BTX-B subjects declared sialorrhea reduction of any kind (moderate for 444 % cases, and dramatic for 333 % subjects), at variance with 611 % controls who denied any benefit from treatment (Chi-square = 229; p < 00001) When present, benefits lasted on average 192 ± 63 weeks in the BTX-B group compared to 67 ± 14 weeks in controls (T-value: 264; p < 00001) BTXB represents a safe and efficacious tool for the management of PDrelated drooling, ensuring a longlasting waning of this disabling symptom

Long-lasting benefits of botulinum toxin type B in Parkinson's disease-related drooling.

The objective of this double-blind, randomized, placebo-controlled study was to test the efficacy of high-dose prednisone, administered as early as possible, in modifying the natural progression of Bell's palsy. Sixty-two consecutive patients, enrolled within 72 hours of facial palsy onset, were assigned to high dose intravenous prednisone in combination with intramuscular polyvitaminic therapy (group A) or polyvitaminic therapy alone (group B). Clinical grading of facial muscle strength and length of absence from work were evaluated. An early worsening of facial muscle strength was observed in controls, leading to the divergence in the trends of the grading scores in the two groups; this result was not confirmed in the long-term follow-up. Treated patients returned to work earlier than controls. In conclusion, early treatment based on high-dose corticosteroids slightly accelerates spontaneous improvement in Bell's palsy.

Influence of early high-dose steroid treatment on Bell's palsy evolution.

Purpose. To assess whether a screening method based on transcranial Doppler (TCD) examination could detect signs of brain hemodynamic impairment in non-insulin-dependent diabetic patients with retinal microangiopathy of varying severity, asymptomatic for cerebrovascular diseases. Methods. We studied 86 patients stratified according to the presence of proliferative diabetic retinopathy (PDR: 29 cases), background retinopathy (BDR: 32 cases) and no diabetic retinopathy (NDR: 25 patients). TCD was performed to record mean flow velocity and pulsatility index values in the middle cerebral (MCA), anterior cerebral (ACA) and ophthalmic arteries (OA), at rest. It was also employed to evaluate the cerebral vasodilatory response to a breath-holding test: the maximum percentage MCA flow velocity increase during the test was taken as an index of cerebrovascular reactivity. Fifty healthy subjects were studied to establish control values. Analysis of variance was used to test inter-group differences. The regression test was applied to define the relationship between TCD parameters and age and disease duration. Results. No significant differences were found between controls and the whole group of patients with respect to TCD parameters. However, subgroup analysis showed PDR patient had a significantly higher pulsatility index and lower cerebrovascular reactivity than BDR and NDR patients. This difference was not explained by the effect of age or disease duration, being greatest in patients under sixty. Conclusions. These findings seem to confirm the hypothesis of a silent cerebral microangiopathy affecting diabetic patients, with concomitant signs of microangiopathic damage in other districts.

Diabetic retinopathy and cerebral hemodynamic impairment in type II diabetes

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