Background and objectiveThe extent to which deep brain stimulation (DBS) can improve quality of life may be perceived as a permanent trade-off between neurological improvements and complications of therapy, comorbidities, and disease progression.Patients and methodsWe retrospectively investigated 123 consecutive and non-preselected patients. Indications for DBS surgery were Parkinson's disease (82), dystonia (18), tremor of different etiology (21), Huntington's disease (1) and Gilles de la Tourette syndrome (1). AEs were defined as any untoward clinical occurrence, sign or patient complaint or unintended disease if related or unrelated to the surgical procedures, implanted devices or ongoing DBS therapy.ResultsOver a mean/median follow-up period of 4.7 years (578 patient-years) 433 AEs were recorded in 106 of 123 patients (86.2%). There was no mortality or persistent morbidity from the surgical procedure. All serious adverse events (SAEs) that occurred within 4 weeks of surgery were reversible. Neurological AEs (193 in 85 patients) and psychiatric AEs (78 in 48 patients) were documented most frequently. AEs in 4 patients (suicide under GPI stimulation, weight gain >20 kg, impairment of gait and speech, cognitive decline >2 years following surgery) were severe or worse, at least possibly related to DBS and non reversible. In PD 23.1% of the STN-stimulated patients experienced non-reversible (or unknown reversibility) AEs that were at least possibly related to DBS in the form of impaired speech or gait, depression, weight gain, cognitive disturbances or urinary incontinence (severity was mild or moderate in 15 of 18 patients). Age and Hoehn&Yahr stage of STN-simulated PD patients, but not preoperative motor impairment or response to levodopa, showed a weak correlation (r = 0.24 and 0.22, respectively) with the number of AEs.ConclusionsDBS-related AEs that were severe or worse and non-reversible were only observed in PD (4 of 82 patients; 4.9%), but not in other diseases. PD patients exhibited a significant risk for non-severe AEs most of which also represented preexisting and progressive axial and non-motor symptoms of PD. Mild gait and/or speech disturbances were rather frequent complaints under VIM stimulation. GPI stimulation for dystonia could be applied with negligible DBS-related side effects.

Although some reports on neurostimulation are positive, no effective treatment method for camptocormia in Parkinson's disease (PD) is known to date. We aim to identify prognostic factors for a beneficial DBS effect on camptocormia. In an observational cohort study, we investigated 25 idiopathic PD patients, who suffered additionally from camptocormia, and underwent bilateral neurostimulation of the subthalamic nucleus (STN) to improve classical PD symptoms. Using an established questionnaire, we examined deep brain stimulation (DBS) effects on camptocormia in addition to general neurostimulation effects. A beneficial neurostimulation effect on camptocormia was defined as an improvement in the bending angle of a least 50%. In 13 patients, the bending angle of camptocormia improved, in 12 patients it did not. A multifactorial analysis revealed a short duration between onset of camptocormia and start of neurostimulation to be the relevant factor for outcome. All patients with duration of camptocormia up to 1.5 years showed a beneficial effect; patients between 1.5 and ∼3 years showed mixed results, but none with a duration of more than 40 months improved except for 1 patient whose camptocormia was levodopa responsive. The bending angle was not a prognostic factor. Our data indicate that the main prognostic factor for a beneficial DBS effect on camptocormia is its short duration. As an explanation, we suggest that neurostimulation may improve camptocormia only as long as muscle pathology is limited. Our findings may help to elucidate the mode of action of neurostimulation. A prospective study is necessary. © 2015 International Parkinson and Movement Disorder Society

Depression, the most common psychiatric complication in Parkinson's disease (PD), affects 40-50 % of PD patients [1]. However, exact epidemiological data are missing. Rates of depression in PD vary between 4 % and 70 % depending on diagnostic criteria and selection of the study population. Application of structured diagnostic interviews (e. g. SCID, MINI, NPI) in non-selected populations would be desirable. Severity of depression and anxiety appears to correlate with disability and reduced quality of life in PD patients. Depression and anxiety appear to be underdiagnosed and undertreated in PD [7], even though adequate diagnosis and treatment affect the course of the disease.The profile of depressive symptoms observed in PD is not identical to that reported in patients with primary depression. Distinctive features of depression in PD include elevated levels of dysphoria, irritability, little guilt or feelings of failure, and a low suicide rate despite a high frequency of suicidal ideation. Diagnosis of depression in PD is complicated by overlapping symptoms of the two disorders. Symptoms of depression including psychomotor slowing and retardation; reduced mimics and apathy may be indistinguishable from neurological motor deficits in PD. Diagnosis of depression in PD is almost exclusively based on subjectively experienced depressive symptoms including: (1) feeling of emptiness and hopelessness, (2) reduced reactivity to emotional stimuli, (3) loss of the ability to enjoy and feel pleasure (anhedonia).Observer-and self-rating depression scales (HAMD, BDI) have been validated in order to assess severity and its course in depressed patients with PD. However, because of overlapping clinical symptoms, available rating scales may not reliably measure severity of depression.Quality of life is rather reduced by subjectively expe-■ Abstract Depression occurs in approximately 45 % of all patients with Parkinson's disease (PD), reduces quality of life independent of motor symptoms and seems to be underrated and undertreated.

Our data indicate that depression in PD is associated with a more pronounced loss of striatal dopamine transporter availability that is most likely secondary to increased dopaminergic degeneration. In addition, depressed PD patients have a lower availability of midbrain/brainstem monoamine transporters than nondepressed PD patients. These findings provide in vivo evidence in support of the known post-mortem data demonstrating more extensive nerve cell loss in PD with depression and indicate that SPECT imaging can help to identify pathophysiological changes underlying nonmotor symptoms in this common movement disorder.

ObjectiveThis pivotal phase III study, SIAXI, investigated the efficacy and safety of incobotulinumtoxinA for the treatment of chronic sialorrhea due to Parkinson disease (PD), atypical parkinsonism, stroke, or traumatic brain injury (TBI).MethodsAdult patients with PD (70.7%), atypical parkinsonism (8.7%), stroke (19.0%), or TBI (2.7%) were randomized (2:2:1) to double-blind treatment with placebo (n = 36), or total doses of incobotulinumtoxinA 75 U (n = 74) or 100 U (n = 74), in a single treatment cycle. The coprimary endpoints were change in unstimulated salivary flow rate from baseline to week 4, and patients' Global Impression of Change Scale score at week 4. Adverse events were recorded throughout.ResultsA total of 184 patients were randomized. Both incobotulinumtoxinA dose groups showed reductions in mean unstimulated salivary flow rate at week 4, with a significant difference vs placebo in the incobotulinumtoxinA 100 U group (p = 0.004). Patients' Global Impression of Change Scale scores also improved at week 4, with a significant difference vs placebo in the incobotulinumtoxinA 100 U group (p = 0.002). A lasting effect was observed at week 16 post injection. The most frequent treatment-related adverse events in the incobotulinumtoxinA 75 U and 100 U groups were dry mouth (5.4% and 2.7% of patients) and dysphagia (2.7% and 0.0% of patients).ConclusionsIncobotulinumtoxinA 100 U is an effective and well-tolerated treatment of chronic sialorrhea in adults.ClinicalTrials.gov identifierNCT02091739.Classification of evidenceThis study provides Class I evidence that incobotulinumtoxinA reduces salivary flow rates in patients with chronic sialorrhea due to PD, atypical parkinsonism, stroke, or TBI.