Impulsivity and Attention in Obsessive Compulsive and Tic Disorders: Mismatch in Self-Report and Behavioural Data.

Impulsivity is a multidimensional, cross-diagnostic behavioural construct that has been described in various psychiatric disorders including obsessive-compulsive disorder (OCD) and Tourette syndrome (TS). Different interpretations of results in the past have raised the question of heightened impulsivity as an explanatory model for self-described impulsive behaviour, especially in OCD. Our study included 16 patients with OCD, 14 patients with TS, and 28 healthy control subjects (HC). Self-assessed impulsivity was examined by the Barratt Impulsiveness Scale-11 (BIS-11), and the behavioural test used was the immediate and delayed memory task (IMT/DMT). Significantly heightened self-assessed impulsivity of the patient collective compared to HC could be observed in in only one dimension: lack of attention (χ2 (2) = 24.910, p < 0.001). Post-hoc tests were performed using Bonferroni adjusted alpha levels of 0.0167 per test (0.05/3) and revealed significantly higher scores in patients with OCD (M = 19.57, SD = 2.82), z = 4.292, p < 0.001 as with TS (M = 19.38, SD = 3.62), z = 3.832, p < 0.001 compared to HC (M = 13.78, SD = 3.18). In patients with OCD, correlations between the dimension of obsessive thoughts with a lack of attention in the form of first-order factor cognitive instability could be shown (n = 14, p = 0.024, rs = 0.599) while in patients with TS, tic symptomatology correlated significantly with second-order factor attentional impulsivity (n = 12, p = 0.027, rs = 0.635). In behavioural testing, no significant group differences could be observed either in impulsive behaviour (IMT: χ2 (2) = 4.709, p = 0.824; DMT: χ2 (2) = 0.126, p = 0.939) or in sustained attention (IMT: χ2 (2) = 0.388, p = 0.095; DMT: χ2 (2) = 0.663, p = 0.718). Heightened impulsivity as an explanatory model for the observed lack of attention, especially in patients with OCD, should be questioned and interpretation biases considered in the future. The necessity of a multidimensional approach to the research of impulsivity is underscored by our results.

Patients with isolated REM-sleep behavior disorder have elevated levels of alpha-synuclein aggregates in stool.

Misfolded and aggregated α-synuclein is a neuropathological hallmark of Parkinson's disease (PD). Thus, α-synuclein aggregates are regarded as a biomarker for the development of diagnostic assays. Quantification of α-synuclein aggregates in body fluids is challenging, and requires highly sensitive and specific assays. Recent studies suggest that α-synuclein aggregates may be shed into stool. We used surface-based fluorescence intensity distribution analysis (sFIDA) to detect and quantify single particles of α-synuclein aggregates in stool of 94 PD patients, 72 isolated rapid eye movement sleep behavior disorder (iRBD) patients, and 51 healthy controls. We measured significantly elevated concentrations of α-synuclein aggregates in stool of iRBD patients versus those of controls (p = 0.024) or PD patients (p < 0.001). Our results show that α-synuclein aggregates are excreted in stool and can be measured using the sFIDA assay, which could support the diagnosis of prodromal synucleinopathies.

Thalamic deep brain stimulation for Tourette Syndrome: A naturalistic trial with brief randomized, double-blinded sham-controlled periods.

BACKGROUND: There is still a lack of controlled studies to prove efficacy of thalamic deep brain stimulation for Tourette's Syndrome. OBJECTIVES: In this controlled trial, we investigated the course of tic severity, comorbidities and quality of life during thalamic stimulation and whether changes in tic severity can be assigned to ongoing compared to sham stimulation. METHODS: We included eight adult patients with medically refractory Tourette's syndrome. Bilateral electrodes were implanted in the centromedian-parafascicular-complex and the nucleus ventro-oralis internus. Tic severity, quality of life and comorbidities were assessed before surgery as well as six and twelve months after. Short randomized, double-blinded sham-controlled crossover sequences with either active or sham stimulation were implemented at both six- and twelve-months' assessments. The primary outcome measurement was the difference in the Yale Global Tic Severity Scale tic score between active and sham stimulation. Adverse events were systematically surveyed for all patients to evaluate safety. RESULTS: Active stimulation resulted in significantly higher tic reductions than sham stimulation (F = 79.5; p = 0.001). Overall quality of life and comorbidities improved significantly in the open-label-phase. Over the course of the trial two severe adverse events occurred that were resolved without sequelae. CONCLUSION: Our results provide evidence that thalamic stimulation is effective in improving tic severity and overall quality of life. Crucially, the reduction of tic severity was primarily driven by active stimulation. Further research may focus on improving stimulation protocols and refining patient selection to improve efficacy and safety of deep brain stimulation for Tourette's Syndrome.

Deep brain stimulation and sensorimotor gating in tourette syndrome and obsessive-compulsive disorder.

Recent translational data suggest that deep brain stimulation (DBS) of the cortico-striato-thalamo-cortical (CSTC) loops improves sensorimotor gating in psychiatric disorders that show deficient prepulse inhibition (PPI), a robust operational measure of sensorimotor gating. To our knowledge we are the first to investigate this effect in patients with Tourette syndrome (TS). We measured PPI of the acoustic startle reflex in patients with TS (N = 10) or Obsessive-Compulsive Disorder (OCD) (N = 8) treated with DBS of the centromedian and ventro-oral internal thalamic nucleus and the anterior limb of internal capsule-nucleus accumbens area respectively, and aged- and gender-matched healthy controls (HC). PPI of the DBS groups was measured in randomized order in the ON and OFF stimulation condition. Statistical analysis revealed no significant difference in PPI (%) of patients with TS between ON (M = 20.5, SD = 14.9) and OFF (M = 25.2, SD = 29.7) condition. There were significantly reduced PPI levels in patients with TS in the ON condition compared to HC (M = 49.2, SD = 10.7), but no significant difference in PPI between TS in the OFF condition and HC. Furthermore, we found no significant stimulation or group effect for OCD and HC (OCD ON: M = 57.0, SD = 8.3; OCD OFF: 67.8, SD = 19.6; HC: M = 63.0, SD = 24.3). Our study has a number of limitations. Sample sizes are small due to the restricted patient collective. The study was not controlled for use of psychoactive medication or nicotine. Furthermore, we were not able to assess presurgical PPI measurements. In conclusion, we were able to show that PPI is impaired in patients with TS. This finding is in line with recent translational work. With respect to the OCD cohort we were not able to replicate our previously published data. A disability in sensorimotor gating plays a pivotal role in many psychiatric disorders therefore more research should be conducted to disentangle the potential and limitations of modulating sensorimotor gating via brain stimulation techniques.