Validation of the Chinese Version of the Questionnaire for Impulsive-Compulsive Disorders in Parkinson's Disease

Background: Impulse control and related disorders (ICRDs) have gained recognition as a severe complication of Parkinson's disease (PD) and are connected to poor quality of life and devastating financial and social problems. This study aimed to evaluate the usefulness of the Questionnaire for Impulsive-Compulsive Disorders in Parkinson's Disease (QUIP) and estimate the risk factors for ICRDs in Chinese patients with PD.Methods: 207 PD patients were assessed using the QUIP and evaluated for PD motor and nonmotor symptoms. ICRDs were diagnosed via interviews of patients or their caregivers, and the clinical characteristics of patients with and without ICRDs were compared.Results: The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of the C-QUIP were 95.0, 83.4, 38.0, 99.4, and 84.5%. The prevalence of each disorder among participants diagnosed via interview was pathological gambling (0.5%), hypersexuality (1.9%), compulsive shopping (1.0%), binge eating (3.9%), hobbyism (1.9%), punding (0.5%), walkabout (0.5%), and dopamine dysregulation syndrome (2.9%). PD patients with ICRDs had longer PD duration, higher Hoehn and Yahr stage, Non-Motor Symptoms Scale (NMSS), and Hamilton-Depression Rating Scale (HAMD). Also, they received a larger total daily levodopa equivalent dose (LED), levodopa dosage, and dopamine agonist only LED (DA-LED) than did PD patients without ICRDs.Conclusions: Given its psychometric properties, the C-QUIP is a valid and rapid screening instrument for assessing of ICRDs in PD patients. Higher Hoehn and Yahr staging, NMSS and HAMD scores, a larger mean LED and levodopa dosage are risk factors for ICRDs.

Levodopa-induced dyskinesia in dementia with Lewy bodies and Parkinson disease with dementia

ObjectiveTo investigate the frequency of levodopa-induced dyskinesia in dementia with Lewy bodies (DLBs) and Parkinson disease with dementia (PDD) and compare these frequencies with patients with incident Parkinson disease (PD) through a population-based cohort study.MethodsWe identified all patients with DLB, PDD, and PD without dementia in a 1991–2010 population-based parkinsonism-incident cohort, in Olmsted County, Minnesota. We abstracted information about levodopa-induced dyskinesia. We compared patients with DLB and PDD with dyskinesia with patients with PD from the same cohort.ResultsLevodopa use and dyskinesia data were available for 141/143 (98.6%) patients with a diagnosis of either DLB or PDD; 87 (61.7%), treated with levodopa. Dyskinesia was documented in 12.6% (8 DLB and 3 PDD) of levodopa-treated patients. Among these patients, median parkinsonism diagnosis age was 74 years (range: 64–80 years); 63.6%, male. The median interval from levodopa initiation to dyskinesia onset was 2 years (range: 3 months–4 years); the median daily levodopa dosage was 600 mg (range: 50–1,600 mg). Dyskinesia severity led to levodopa adjustments in 5 patients, and all improved. Patients with dyskinesia were diagnosed with parkinsonism at a significantly younger age compared with patients without dyskinesia (p < 0.001). Levodopa dosage was unrelated to increased risk of dyskinesias among DLB and PDD. In contrast, 30.1% of levodopa-treated patients with PD developed dyskinesia. In age-, sex-, and levodopa dosage–adjusted models, Patients with DLB and PDD each had lower odds of developing dyskinesia than patients with PD (odds ratio = 0.42, 95% CI 0.21–0.88; p = 0.02).ConclusionsThe dyskinesia risk for levodopa-treated patients with DLB or PDD was substantially less than for levodopa-treated patients with PD.

Parkinsonism Treatment for Those Already on Medications

The previous chapter provided instructions for starting and adjusting carbidopa/levodopa, but specifically pertained to those individuals on no other drugs for parkinsonism or those on only a low carbidopa/levodopa dosage. In this chapter, we focus on people who are taking other drugs for parkinsonism either with or without carbidopa/levodopa. As mentioned earlier, people with DLB or PDD are prone to hallucinations and delusions, which can be exacerbated by drugs for parkinsonism. Carbidopa/levodopa is the least likely to worsen or provoke these problems; however, this is true only if it is used alone (i.e., without other parkinsonism drugs). Carbidopa/levodopa is also the most efficacious drug for parkinsonism. Thus it is reasonable to take the approach that carbidopa/levodopa should be the sole treatment for parkinsonism in DLB or PDD. Whereas using carbidopa/levodopa by itself is often tolerated, adding it to other parkinsonian medications may provoke problems, especially hallucinations or delusions. Hence, before starting carbidopa/levodopa, it is wise to scrutinize the medication list and eliminate other parkinsonism drugs, one by one. There are two general rules of thumb regarding these medications: 1 It is not necessary to change drugs if things are going well and are expected to continue. 2 Change only one medication at a time (but if there are severe drug side effects, the physician may take more aggressive action). Some drugs are worse offenders than others and will be prioritized with that in mind. Note that a variety of schemes may be employed to taper off a drug. The drug-elimination schedules provided below are somewhat arbitrary and other similar schedules may work as well. The most important factor is the total time to reduce the dosage down to zero. The longer a person has been on a medication and the higher the dosage, the more prolonged the taper. The clinician needs to work closely with the patient as this is being done. Parkinsonism may transiently worsen when these drugs are eliminated; however, this typically can subsequently be reversed with carbidopa/levodopa adjustments.

Intensive Rehabilitation Treatment in Parkinsonian Patients with Dyskinesias: A Preliminary Study with 6-Month Followup

A major adverse effect of levodopa therapy is the development of dyskinesia, which affects 30–40% of chronically treated Parkinsonian patients. We hypothesized that our rehabilitation protocol might allow a reduction in levodopa dosage without worsening motor performances, thus reducing frequency and severity of dyskinesias. Ten Parkinsonian patients underwent a 4-week intensive rehabilitation treatment (IRT). Patients were evaluated at baseline, at the end of the rehabilitation treatment and at 6-month followup. Outcome measures were the Unified Parkinson’s Disease Rating Scale Sections II, III, and IV (UPDRS II, III, IV) and the Abnormal Involuntary Movement Scale (AIMS). At the end of the IRT, levodopa dosage was significantly reduced (P=0.0035), passing from1016±327to777±333 mg/day. All outcome variables improved significantly (P<0.0005all) by the end of IRT. At followup, all variables still maintained better values with respect to admission (P<0.02all). In particular AIMS score improved passing from11.90±6.5at admission to3.10±2.3at discharge and to4.20±2.7at followup. Our results suggest that it is possible to act on dyskinesias in Parkinsonian patients with properly designed rehabilitation protocols. Intensive rehabilitation treatment, whose acute beneficial effects are maintained over time, might be considered a valid noninvasive therapeutic support for Parkinsonian patients suffering from diskinesia, allowing a reduction in drugs dosage and related adverse effects.